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  • BioEssays  (220)
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  • 1
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    BioEssays 1∕2015 (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-12-18
    Print ISSN: 0265-9247
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  • 2
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    BioEssays 12∕2014 (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-11-11
    Description: Dynamic interactions with DNA allow replication protein A to direct single-stranded DNA-intermediates into different pathways for synthesis or repair. On pages 1156–1161 , Chen and Wold review recent discoveries that show that replication protein A (RPA), the major eukaryotic single-stranded DNA-binding protein, binds DNA dynamically and that this is important for correct processing of DNA intermediates. The cover shows a model of human RPA interacting with ssDNA based on the known structures of the domains of human RPA and the structure of Ustalago RPA bound to DNA. The three subunits of RPA are shown in blue (RPA1), red (RPA2), and green (RPA3) with ssDNA shown in black.
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  • 3
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    BioEssays – Next Issue (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-11-11
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  • 4
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    Is microbial gardening a food gamble or a safe bet? (Comment on DOI 10.1002/bies.201400100) (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-11-11
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  • 5
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    A word of heartfelt thanks to our reviewers (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-11-11
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  • 6
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    Xenotransplantation exposes the etiology of azoospermia factor (AZF) induced male sterility (2014)
    Wiley
    In: BioEssays
    Details
    Publication Date: 2014-12-19
    Description: Ramathal et al. have employed an elegant xenotransplantation technique to study the fate of human induced pluripotent stem cells (hiPSCs) from fertile males and from males carrying Y chromosome deletions of the azoospermia factor ( AZF ) region. When placed in a mouse testis niche, hiPSCs from fertile males differentiate into germ cell-like cells (GCLCs). Highlighting the crucial role of cell autonomous factors in male sterility, hiPSCs derived from azoospermic males prove to be less successful under similar circumstances. Their studies argue that the agametic “Sertoli cell only” phenotype of two of the AZF deletions likely arises from a defect in the maintenance of germline stem cells (GSCs) rather than from a defect in their specification. These observations underscore the importance of the dialogue between the somatic niche and its inhabitant stem cells, and open up interesting questions concerning the functioning of the somatic niche and how it communicates to the GSCs. In Ramathal et al., human induced pluripotent stem cells (hiPSCs) from wild type and azoospermic men adopt germ cell fate in vitro. Upon xenotransplantation into mouse seminiferous tubules, these hiPSCs acquired germ cell-like (GCL) fate. Remarkably, samples from azoospermic males were less efficient in both contexts.
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  • 7
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    Promoter or enhancer, what's the difference? Deconstruction of established distinctions and presentation of a unifying model (2014)
    Wiley
    In: BioEssays
    Details
    Publication Date: 2014-12-03
    Description: Gene transcription is strictly controlled by the interplay of regulatory events at gene promoters and gene-distal regulatory elements called enhancers. Despite extensive studies of enhancers, we still have a very limited understanding of their mechanisms of action and their restricted spatio-temporal activities. A better understanding would ultimately lead to fundamental insights into the control of gene transcription and the action of regulatory genetic variants involved in disease. Here, I review and discuss pros and cons of state-of-the-art genomics methods to localize and infer the activity of enhancers. Among the different approaches, profiling of enhancer RNAs yields the highest specificity and may be superior in detecting in vivo activity. I discuss their apparent similarities to promoters, which challenge the established view of enhancers and promoters as distinct entities, and present a unifying model of regulatory elements in transcriptional regulation, in which activity, transcriptional output and regulatory function is context specific. Profiling of enhancer RNAs (eRNAs) likely represents a paradigm shift in enhancer genomics, yielding high specificity in the localization of active enhancers. The similarities between enhancers and promoters are discussed and their established distinctions are deconstructed. Based on this, a unified model of regulatory elements in transcriptional regulation is presented.
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  • 8
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    BioEssays 2∕2014 (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-01-15
    Description: Comparing structural and evolutionary dynamics of proteins . On pages 209–218 Marsh and Teichmann discuss parallels between protein dynamics and evolution, and how we can gain insights into function from these studies. Buried residues, for example, are usually more evolutionarily conserved and evolve less quickly than exposed residues. These residues generally form more intramolecular contacts, and mutating them would therefore more likely lead to a destabilization of the protein. Having more intramolecular contacts on the other hand also means that these residues are less flexible to move around. In contrast, dynamic parts of a protein in real time are also dynamic over evolutionary time and evolve more quickly. The cover shows the buried (blue) and surface (red) residues for the receiver domain of sensor histidine kinase CKI1 from Arabidopsis .
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  • 9
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    BioEssays 2∕2014 (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-01-15
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  • 10
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    BioEssays – Next Issue (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-01-15
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  • 11
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    Epigenetic programing of depression during gestation (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-01-22
    Description: Gestational factors play a role in the development of several neuropsychiatric disorders including schizophrenia and autism. In utero conditions influence future mental health through epigenetic mechanisms, which alter gene expression without affecting DNA coding sequence. Environmental factors account for at least 60% of the risk for developing major depression, and earlier onset of depressive illness has been observed over the past decades. I speculate that gestational factors may play a greater role in programing depression than previously recognized. Here, I examine recent evidence for a role for gestational factors in programing mood disorders, and how epigenetic mechanisms mediate this effect. How does the gestational environment transduce vulnerability to depression to the fetus? The in utero environment alters gene expression through epigenetic mechanisms, which mediate long-term effects on physiology and behavior without changing DNA sequence. I examine recent work suggesting that gestational environment programs depression in adult offspring via epigenetics.
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  • 12
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    Do all creatures possess an acquired immune system of some sort? (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-01-15
    Description: Recent findings have provided evidence for the existence of non-vertebrate acquired immunity. We survey these findings and propose that all living organisms must express both innate and acquired immunity. This is opposed to the paradigm that only vertebrates manifest the two forms of immune mechanism; other species are thought to use innate immunity alone. We suggest new definitions of innate and acquired immunity, based on whether immune recognition molecules are encoded in the inherited genome or are generated through somatic processes. We reason that both forms of immunity are similarly ancient, and have co-evolved in response to lifestyle, cost-benefit tradeoffs and symbiosis versus parasitism. However, different species have evolved different immune solutions that are not necessarily genetically related, but serve a similar general function – allowing individuals to learn from their own immune experience; survival of species is contingent on the acquired immune experience of its individuals. We propose that all organisms express both innate and adaptive/acquired immunity. Acquired immune manifestations vary between species, but all use recognition molecules not directly encoded in the inherited genome, and all serve a similar function – allowing individuals to learn from their own immune experience, thus promoting species survival.
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  • 13
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    From the selfish gene to selfish metabolism: Revisiting the central dogma (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-01-15
    Description: The standard representation of the Central Dogma (CD) of Molecular Biology conspicuously ignores metabolism. However, both the metabolites and the biochemical fluxes behind any biological phenomenon are encrypted in the DNA sequence. Metabolism constrains and even changes the information flow when the DNA-encoded instructions conflict with the homeostasis of the biochemical network. Inspection of adaptive virulence programs and emergence of xenobiotic-biodegradation pathways in environmental bacteria suggest that their main evolutionary drive is the expansion of their metabolic networks towards new chemical landscapes rather than perpetuation and spreading of their DNA sequences. Faulty enzymatic reactions on suboptimal substrates often produce reactive oxygen species (ROS), a process that fosters DNA diversification and ultimately couples catabolism of the new chemicals to growth. All this calls for a revision of the CD in which metabolism (rather than DNA) has the leading role. The central dogma of Molecular Biology has shortcomings that need revision: (i) metabolism is the next step of the information flow, (ii) metabolism has the predominant role (thereby the hierarchy of actors should be flipped upside down) and (iii) metabolism feedbacks on DNA by means of reactive oxygen species.
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  • 14
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    BioEssays 2∕2014 (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-01-15
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  • 15
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    Transfer and functional consequences of dietary microRNAs in vertebrates: Concepts in search of corroboration (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-01-17
    Description: If validated, diet-derived foreign microRNA absorption and function in consuming vertebrates would drastically alter our understanding of nutrition and ecology. RNA interference (RNAi) mechanisms of Caenorhabditis elegans are enhanced by uptake of environmental RNA and amplification and systemic distribution of RNAi effectors. Therapeutic exploitation of RNAi in treating human disease is difficult because these accessory processes are absent or diminished in most animals. A recent report challenged multiple paradigms, suggesting that ingested microRNAs (miRNAs) are transferred to blood, accumulate in tissues, and exert canonical regulation of endogenous transcripts. Independent replication of these findings has been elusive, and multiple disconfirmatory findings have been published. In the face of mounting negative results, any additional positive reports must provide the proverbial “extraordinary proof” to support such claims. In this article, we review the evidence for and against a significant role for dietary miRNAs in influencing gene expression, and make recommendations for future studies. A report that foreign microRNAs from the diet rival endogenous vertebrate miRNAs in abundance and function has been refuted by multiple independent studies, although low-level uptake may occur. We present the current evidence for and against the paradigm-challenging but uncorroborated dietary xenomiR hypothesis, and discuss remaining questions in the field.
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  • 16
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    A paternal environmental legacy: Evidence for epigenetic inheritance through the male germ line (2014)
    Wiley
    In: BioEssays
    Details
    Publication Date: 2014-01-17
    Description: Literature on maternal exposures and the risk of epigenetic changes or diseases in the offspring is growing. Paternal contributions are often not considered. However, some animal and epidemiologic studies on various contaminants, nutrition, and lifestyle-related conditions suggest a paternal influence on the offspring's future health. The phenotypic outcomes may have been attributed to DNA damage or mutations, but increasing evidence shows that the inheritance of environmentally induced functional changes of the genome, and related disorders, are (also) driven by epigenetic components. In this essay we suggest the existence of epigenetic windows of susceptibility to environmental insults during sperm development. Changes in DNA methylation, histone modification, and non-coding RNAs are viable mechanistic candidates for a non-genetic transfer of paternal environmental information, from maturing germ cell to zygote. Inclusion of paternal factors in future research will ultimately improve the understanding of transgenerational epigenetic plasticity and health-related effects in future generations. Animal and epidemiologic studies on various environmental exposures suggest that transgenerational epigenetic changes can be induced through the paternal germ line, ultimately affecting health status of the offspring. This essay suggests the existence of epigenetic windows of susceptibility to environmental insults during spermatogenesis or other early developmental processes.
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  • 17
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    Explaining general anesthesia: A two-step hypothesis linking sleep circuits and the synaptic release machinery (2014)
    Wiley
    In: BioEssays
    Details
    Publication Date: 2014-01-23
    Description: Several general anesthetics produce their sedative effect by activating endogenous sleep pathways. We propose that general anesthesia is a two-step process targeting sleep circuits at low doses, and synaptic release mechanisms across the entire brain at the higher doses required for surgery. Our hypothesis synthesizes data from a variety of model systems, some which require sleep (e.g. rodents and adult flies) and others that probably do not sleep (e.g. adult nematodes and cultured cell lines). Non-sleeping systems can be made insensitive (or hypersensitive) to some anesthetics by modifying a single pre-synaptic protein, syntaxin1A. This suggests that the synaptic release machinery, centered on the highly conserved SNARE complex, is an important target of general anesthetics in all animals. A careful consideration of SNARE architecture uncovers a potential mechanism for general anesthesia, which may be the primary target in animals that do not sleep, but a secondary target in animals that sleep. Volatile general anesthetics such as isoflurane produce loss of behavioral responsiveness in all animals. We propose that this can be explained as a two-step process: activation of endogenous sleep pathways at low doses followed by attenuation of synaptic release at the drug concentrations required for surgery.
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  • 18
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    Ancient biomolecules: Their origins, fossilization, and role in revealing the history of life (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-03-14
    Description: The discovery of traces of a blood meal in the abdomen of a 50-million-year-old mosquito reminds us of the insights that the chemistry of fossils can provide. Ancient DNA is the best known fossil molecule. It is less well known that new fossil targets and a growing database of ancient gene sequences are paralleled by discoveries on other classes of organic molecules. New analytical tools, such as the synchrotron, reveal traces of the original composition of arthropod cuticles that are more than 400 my old. Pigments such as melanin are readily fossilized, surviving virtually unaltered for ∼200 my. Other biomarkers provide evidence of microbial processes in ancient sediments, and have been used to reveal the presence of demosponges, for example, more than 635 mya, long before their spicules appear in the fossil record. Ancient biomolecules are a powerful complement to fossil remains in revealing the history of life. Ancient biomolecules range from hundreds of thousand-year-old DNA to lipids and structural macromolecules that survive for billions of years. Extracted from fossils and sedimentary rocks, they reveal organism relationships, past environments, and the origin of fossil fuels. In the oldest rocks they may be the only evidence of particular life forms.
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  • 19
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    European do-it-yourself (DIY) biology: Beyond the hope, hype and horror (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-04-30
    Description: The encounter of amateur science with synthetic biology has led to the formation of several amateur/do-it-yourself biology (DIYBio) groups worldwide. Although media outlets covered DIYBio events, most seemed only to highlight the hope, hype, and horror of what DIYBio would do in the future. Here, we analyze the European amateur biology movement to find out who they are, what they aim for and how they differ from US groups. We found that all groups are driven by a core leadership of (semi-)professional people who struggle with finding lab space and equipment. Regulations on genetic modification limit what groups can do. Differences between Europe and the US are found in the distinct regulatory environments and the European emphasis on bio-art. We conclude that DIYBio Europe has so far been a responsible and transparent citizen science movement with a solid user base that will continue to grow irrespective of media attention. Here, we analyzed the European do-it-yourself biology (DIYBio) community consisting of enthusiastic biotechnologists, artists, and designers. We conclude that DIYBio Europe has so far been a responsible and transparent citizen science movement with a solid user base that will continue to grow irrespective of media attention.
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  • 20
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    Keeping your armour intact: How HIV-1 evades detection by the innate immune system (2014)
    Wiley
    In: BioEssays
    Details
    Publication Date: 2014-04-30
    Description: HIV-1 infects dendritic cells (DCs) without triggering an effective innate antiviral immune response. As a consequence, the induction of adaptive immune responses controlling virus spread is limited. In a recent issue of Immunity , Lahaye and colleagues show that intricate interactions of HIV capsid with the cellular cofactor cyclophilin A (CypA) control infection and innate immune activation in DCs. Manipulation of HIV-1 capsid to increase its affinity for CypA results in reduced virus infectivity and facilitates access of the cytosolic DNA sensor cGAS to reverse transcribed DNA. This in turn induces a strong host response. Here, we discuss these findings in the context of recent developments in innate immunity and consider the implications for disease control and vaccine design. Cellular proteins including cyclophilin A (CypA) interact with the capsid (CA) of HIV-1. Recent work shows that wild-type CA prevents the induction of an interferon (IFN) response. Increased CypA binding to mutated CA results in abortive infection and activation of the innate immune sensor cGAS that detects exposed cDNA.
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  • 21
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    Beyond inhibition: GABA synapses tune the neuroendocrine stress axis (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-03-20
    Description: We recently described a novel form of stress-associated bidirectional plasticity at GABA synapses onto hypothalamic parvocellular neuroendocrine cells (PNCs), the apex of the hypothalamus-pituitary-adrenal axis. This plasticity may contribute to neuroendocrine adaptation. However, this GABA synapse plasticity likely does not translate into a simple more and less of inhibition because the ionic driving force for Cl − , the primary charge carrier for GABA A receptors, is dynamic. Specifically, stress impairs a Cl − extrusion mechanism in PNCs. This not only renders the steady-state GABA response less hyperpolarizing but also makes PNCs susceptible to the activity-dependent accumulation of Cl − . Accordingly, GABA synapse plasticity impacts both the robustness of GABA voltage response and dynamic Cl − loading, imposing nonlinear influences on PNC excitability during circuit activities. This theoretical consideration predicts roles for GABA transmission far more versatile than canonical inhibition. We propose potential impacts of GABA synapse plasticity on the experience-dependent fine-tuning of neuroendocrine stress responses. Hypothalamic parvovellular neuroendocrine cells (PNCs) form the apex of the hypothalamus-pituitary-adrenal axis, controlling the corticosteroid (CORT) response to stress. GABAergic inputs onto PNCs undergo multiple forms of plasticity following stress. We propose a hypothesis that GABA synapse plasticity impacts Cl − homeostasis, generates excitatory GABA responses, and tunes neuroendocrine response.
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  • 22
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    Chromosome replication origins: Do we really need them? (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-03-20
    Description: Replication of the main chromosome in the halophilic archaeon Haloferax volcanii was recently reported to continue despite deletion of all active replication origins. Equally surprising, the deletion strain grew faster than the parent strain. It was proposed that origin-less H. volcanii duplicate their chromosomes via recombination-dependent replication. Here, we recall our present knowledge of this mode of chromosome replication in different organisms. We consider the likelihood that it accounts for the viability of H. volcanii deleted for its main specific replication origins, as well as possible alternative interpretations of the results. The selective advantages of having defined chromosome replication origins are discussed from a functional and evolutionary perspective. Hawkins et al. (Nature 503:544–7, 2013) reported the surprising finding that deleting all three replication origins from the archaea Haloferax volcanii main chromosome does not impair viability and rather increases growth rate. We discuss the authors' proposal that replication is then initiated from recombination intermediates, and present alternative hypotheses.
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  • 23
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    Biology of purinergic signalling: Its ancient evolutionary roots, its omnipresence and its multiple functional significance (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-05-01
    Description: The purinergic signalling system, which utilises ATP, related nucleotides and adenosine as transmitter molecules, appeared very early in evolution: release mechanisms and ATP-degrading enzymes are operative in bacteria, and the first specific receptors are present in single cell eukaryotic protozoa and algae. Further evolution of the purinergic signalling system resulted in the development of multiple classes of purinoceptors, several pathways for release of nucleotides and adenosine, and a system of ectonucleotidases controlling extracellular levels of purinergic transmitters. The purinergic signalling system is expressed in virtually all types of tissues and cells, where it mediates numerous physiological reactions and contributes to pathological responses in a variety of diseases. Purinergic chemical signalling appears early in evolution in species without a nervous system followed by purinergic neurotransmission in animals that developed a nervous system. Widespread purinoceptor expression on most mammalian cell types suggests ATP and adenosine have been retained as successful, compared to more restricted distributions of other chemical messengers.
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  • 24
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    Aging genomes: A necessary evil in the logic of life (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-01-26
    Description: Genomes are inherently unstable because of the need for DNA sequence variation as a substrate for evolution through natural selection. However, most multicellular organisms have postmitotic tissues, with limited opportunity for selective removal of cells harboring persistent damage and deleterious mutations, which can therefore contribute to functional decline, disease, and death. Key in this process is the role of genome maintenance, the network of protein products that repair DNA damage and signal DNA damage response pathways. Genome maintenance is beneficial early in life by swiftly eliminating DNA damage or damaged cells, facilitating rapid cell proliferation. However, at later ages accumulation of unrepaired damage and mutations, as well as ongoing cell depletion, promotes cancer, atrophy, and other deleterious effects associated with aging. As such, genome maintenance and its phenotypic sequelae provide yet another example of antagonistic pleiotropy in aging and longevity. DNA damage has since long been suspected to be a major cause of aging. Here, I will discuss the dual role of genome maintenance systems in providing DNA sequence variation in the germline as the substrate for evolution and mediating DNA damage-induced aging phenotypes in the soma.
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  • 25
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    Distinct mechanisms determine organ left-right asymmetry patterning in an uncoupled way (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-01-26
    Description: Disruption of Nodal in the lateral plate mesoderm (LPM) usually leads to left-right (LR) patterning defects in multiple organs. However, whether the LR patterning of organs is always regulated in a coupled way has largely not yet been elucidated. In addition, whether other crucial regulators exist in the LPM that coordinate with Nodal in regulating organ LR patterning is also undetermined. In this paper, after briefly summarizing the common process of LR patterning, the most puzzling question regarding the initiation of asymmetry is considered and the divergent mechanisms underlying the uncoupled LR patterning in different organs are discussed. On the basis of cases in which different organ LR patterning is determined in an uncoupled way via an independent mechanism or at a different time, we propose that there are other critical factors in the LPM that coordinate with Nodal to regulate heart LR asymmetry patterning during early LR patterning. Also watch the Video Abstract . Based on the fact that distinct mechanisms determine different organ left-right (LR) patterning in an uncoupled way, we hypothesize that other critical factors in the lateral plate mesoderm (LPM) may coordinate with Nodal to regulate heart LR asymmetry patterning during LR patterning, and this can be evaluated by our proposed model.
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  • 26
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    Diversity through duplication: Whole-genome sequencing reveals novel gene retrocopies in the human population (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-02-26
    Description: Gene retrocopies are generated by reverse transcription and genomic integration of mRNA. As such, retrocopies present an important exception to the central dogma of molecular biology, and have substantially impacted the functional landscape of the metazoan genome. While an estimated 8,000–17,000 retrocopies exist in the human genome reference sequence, the extent of variation between individuals in terms of retrocopy content has remained largely unexplored. Three recent studies by Abyzov et al., Ewing et al. and Schrider et al. have exploited 1,000 Genomes Project Consortium data, as well as other sources of whole-genome sequencing data, to uncover novel gene retrocopies. Here, we compare the methods and results of these three studies, highlight the impact of retrocopies in human diversity and genome evolution, and speculate on the potential for somatic gene retrocopies to impact cancer etiology and genetic diversity among individual neurons in the mammalian brain. Three recent studies have employed whole genome sequencing data to identify novel gene retrocopies in humans, by exploiting distinguishing retrocopy hallmarks including exon-exon junctions and genomic locations distal to parent genes. Gene retrocopies contribute to human genetic diversity.
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  • 27
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    Early life epigenetic programming and transmission of stress-induced traits in mammals (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-03-01
    Description: The environment can have a long-lasting influence on an individual's physiology and behavior. While some environmental conditions can be beneficial and result in adaptive responses, others can lead to pathological behaviors. Many studies have demonstrated that changes induced by the environment are expressed not only by the individuals directly exposed, but also by the offspring sometimes across multiple generations. Epigenetic alterations have been proposed as underlying mechanisms for such transmissible effects. Here, we review the most relevant literature on these changes and the developmental stages they affect the most. We discuss current evidence for transgenerational effects of prenatal and postnatal factors on bodily functions and behavioral responses, and the potential epigenetic mechanisms involved. We also discuss the need for a careful evaluation of the evolutionary importance with respect to health and disease, and possible directions for future research in the field. Evidence for epigenetic inheritance of acquired traits in mammals is growing. Transgenerational transmission is based on mechanisms involving DNA-methylation, histone post-translational modifications, and non-coding small RNAs in the germline. These epigenetic modifications constitute potential vehicles for effects of early life stress and nutrition on brain and behavior across generations.
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    The mark of metabolism: Another nail in the coffin of nucleic-acids-first in the origin of life? (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-02-07
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    BioEssays 3∕2014 (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-02-07
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    Opening the genetic toolbox of niche model organisms with high throughput techniques: Novel proteins in regeneration as a case study (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-02-13
    Description: Understanding in vivo regeneration of complex structures offers a fascinating perspective for translation into medical applications. Unfortunately, mammals in general lack large-scale regenerative capacity, whereas planarians, newts or Hydra can regenerate complete body parts. Such organisms are, however, poorly annotated because of the lack of sequence information. This leads to limited access for molecular biological investigations. In the last decade, high throughput technologies and new methods enabling the effective generation of transgenic animals have rapidly evolved. These developments have allowed the extensive use of niche model organisms as part of a trend towards the accessibility of a greater panel of model species for scientific research. The case study that follows provides an insight into the impact of high throughput techniques on the landscape of models of regeneration. The cases presented here give evidence of alternative stem cell maintenance pathways, the identification of new protein families and new stem cell markers. Regeneration of complex structures is a capability mastered by a small number of niche model organisms. Although such organisms are poorly annotated, current technologies allow the extensive use of such organisms. Representative studies give evidence of alternative stem cell maintenance pathways, new protein families, and new stem cell markers.
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    Unravelling the developmental regulatory networks in early animals (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-02-23
    Description: Development, life cycle evolution and immunity were among the topics discussed at a recent meeting in Tutzing dedicated to the biology of the ‘basal’ metazoan taxa Porifera, Ctenophora, Placozoa and Cnidaria.
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    Clustered and genome-wide transient mutagenesis in human cancers: Hypermutation without permanent mutators or loss of fitness (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-02-27
    Description: The gain of a selective advantage in cancer as well as the establishment of complex traits during evolution require multiple genetic alterations, but how these mutations accumulate over time is currently unclear. There is increasing evidence that a mutator phenotype perpetuates the development of many human cancers. While in some cases the increased mutation rate is the result of a genetic disruption of DNA repair and replication or environmental exposures, other evidence suggests that endogenous DNA damage induced by AID/APOBEC cytidine deaminases can result in transient localized hypermutation generating simultaneous, closely spaced (i.e. “clustered”) multiple mutations. Here, we discuss mechanisms that lead to mutation cluster formation, the biological consequences of their formation in cancer and evidence suggesting that APOBEC mutagenesis can also occur genome-wide. This raises the possibility that dysregulation of these enzymes may enable rapid malignant transformation by increasing mutation rates without the loss of fitness associated with permanent mutators. Some environmental agents and APOBEC cytidine deaminases result in transient hypermutation by causing lesions in ssDNA regions within double strand break repair intermediates and at replication forks. In human cancers such multiple lesions produce mutation clusters, also termed kataegis. Hypermutation of multiple simultaneously formed ssDNA regions may accelerate cancer development.
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    Genetic instability is prevented by Mrc1-dependent spatio-temporal separation of replicative and repair activities of homologous recombination (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-02-27
    Description: Homologous recombination (HR) is required to protect and restart stressed replication forks. Paradoxically, the Mrc1 branch of the S phase checkpoints, which is activated by replicative stress, prevents HR repair at breaks and arrested forks. Indeed, the mechanisms underlying HR can threaten genome integrity if not properly regulated. Thus, understanding how cells avoid genetic instability associated with replicative stress, a hallmark of cancer, is still a challenge. Here I discuss recent results that support a model by which HR responds to replication stress through replicative and repair activities that operate at different stages of the cell cycle (S and G2, respectively) and in distinct subnuclear structures. Remarkably, the replication checkpoint appears to control this scenario by inhibiting the assembly of HR repair centers at stressed forks during S phase, thereby avoiding genetic instability. Homologous recombination proteins Rad52/BRCA2 and Rad51 escort and help stressed replication forks. I propose that the Mrc1-dependent checkpoint restricts recombinational repair to G2 by inhibiting the assembly of repair centers at stressed forks, a scenario that would interfere with proper replication and might promote fork restart by detrimental recombinogenic events.
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    H3.3 turnover: A mechanism to poise chromatin for transcription, or a response to open chromatin? (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-04-04
    Description: Histone H3.3 turnover displays distinct dynamics at various genomic elements such as promoters, enhancers, gene bodies, and heterochromatic regions, suggesting that it is differentially regulated according to chromatin context. Incorporation of variant histones into chromatin provides a mechanism to modulate chromatin states in addition to histone modifications. The replication-independent deposition and replacement of histone variant H3.3, i.e. H3.3 turnover, is mainly associated with transcriptional activity. H3.3 or H3.3-like histone turnover has been studied in various organisms from yeast to mammals. Here, we review the recent progress on this topic. The diversified turnover profiles of H3.3, and their corresponding underlying mechanisms, may reflect distinct requirements for chromatin accessibility in different biological events. Histone H3.3 turnover displays distinct dynamics at various genomic elements such as promoters, enhancers, gene bodies, and heterochromatic regions. The diversified turnover profiles of H3.3, and their corresponding underlying mechanisms, may reflect distinct requirements for chromatin accessibility in different biological events.
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    The alien replicon: Artificial genetic constructs to direct the synthesis of transmissible self-replicating RNAs (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-09-03
    Description: Artificial genetic constructs that direct the synthesis of self-replicating RNA molecules are used widely to induce gene silencing, for bioproduction, and for vaccination. Interestingly, one variant of the self-replicon has not been discussed in the literature: namely, transgenic organisms that synthesise alien replicons. For example, plant cells may be easily genetically modified to produce bacteriophages or insect viruses. Alien replicon-producing organisms (ARPOs) may serve as a unique tool for biocontrol or to selectively influence the characteristics of a target organism. The ARPO approach would have to meet strict biosafety criteria, and its practical applications are problematic. However, a discussion on ARPO applicability would be valuable to outline the full set of options available in the bioengineering toolbox. In this paper, RNA replicons for bioengineering are reviewed briefly, and the ARPO approach is discussed. Genetic construct produces two mRNAs: for viral replicon (1), and for corresponding coat protein (2). Coat protein (3) specifically packs the replicon mRNA into transmissible virus-like particles. Plants interact with a target organism susceptible for this virus and the replicon may spread over its population.
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    SHIP2 phosphatase domain structure suggests sites of regulation (retrospective on DOI 10.1002/bies.201100195) (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-09-25
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    Identifying (non-)coding RNAs and small peptides: Challenges and opportunities (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-10-25
    Description: Over the past decade, high-throughput studies have identified many novel transcripts. While their existence is undisputed, their coding potential and functionality have remained controversial. Recent computational approaches guided by ribosome profiling have indicated that translation is far more pervasive than anticipated and takes place on many transcripts previously assumed to be non-coding. Some of these newly discovered translated transcripts encode short, functional proteins that had been missed in prior screens. Other transcripts are translated, but it might be the process of translation rather than the resulting peptides that serves a function. Here, we review annotation studies in zebrafish to discuss the challenges of placing RNAs onto the continuum that ranges from functional protein-encoding mRNAs to potentially non-functional peptide-producing RNAs to non-coding RNAs. As highlighted by the discovery of the novel signaling peptide Apela/ELABELA/Toddler, accurate annotations can give rise to exciting opportunities to identify the functions of previously uncharacterized transcripts. There is accumulating evidence that translation occurs at many sites outside of known protein-coding regions. This phenomenon of pervasive translation presents a challenge for gene annotations, but also gives rise to exciting opportunities to identify functions for uncharacterized genes.
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    Histone proteolysis: A proposal for categorization into ‘clipping’ and ‘degradation’ (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-10-29
    Description: We propose for the first time to divide histone proteolysis into “histone degradation” and the epigenetically connoted “histone clipping”. Our initial observation is that these two different classes are very hard to distinguish both experimentally and biologically, because they can both be mediated by the same enzymes. Since the first report decades ago, proteolysis has been found in a broad spectrum of eukaryotic organisms. However, the authors often not clearly distinguish or determine whether degradation or clipping was studied. Given the importance of histone modifications in epigenetic regulation we further elaborate on the different ways in which histone proteolysis could play a role in epigenetics. Finally, unanticipated histone proteolysis has probably left a mark on many studies of histones in the past. In conclusion, we emphasize the significance of reviving the study of histone proteolysis both from a biological and an experimental perspective. Also watch the Video Abstract . By categorizing histone proteolysis into “Histone Clipping” and “Histone Degradation” we illustrate that these biologically diverse processes are mediated by the same enzymes, such as Cathepsin L and Neutrophil Elastase. Experimentally distinguishing both classes is a prerequisite to define the role of histone clipping in epigenetics in the future.
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    Meeting report: The road to science-based policy – ESOF through the eyes of young scientists (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-10-28
    Description: Communication and common understanding between politicians, scientists, and the society can lead to evidence-based science policy, a core principle that guides high caliber research and open innovation for a sustainable future.
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    Confidence, tolerance, and allowance in biological engineering: The nuts and bolts of living things (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-10-28
    Description: The emphasis of systems and synthetic biology on quantitative understanding of biological objects and their eventual re-design has raised the question of whether description and construction standards that are commonplace in electric and mechanical engineering are applicable to live systems. The tuning of genetic devices to deliver a given activity is generally context-dependent, thereby undermining the re-usability of parts, and predictability of function, necessary for manufacturing new biological objects. Tolerance (acceptable limits within the unavoidable divergence of a nominal value) and allowance (deviation introduced on purpose for the sake of flexibility and hence modularity, i.e. fitting together with a variety of other components) are key aspects of standardization that need to be brought to biological design. These should endow functional building blocks with a pre-specified level of confidence for bespoke biosystems engineering. However, in the absence of more fundamental knowledge, fine-tuning necessarily relies on evolutionary/combinatorial gravitation toward a fixed objective. Assembly of functional objects within a pre-existing frame might happen through forced standardization of the boundaries (A), through joining interacting parts with flexible interfaces permitting allowance and tolerance (B) or random exploration of a solution space (C). We argue that this is true both for mechanical engineering and synthetic biology.
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    Does RNA editing compensate for Alu invasion of the primate genome? (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-11-01
    Description: One of the distinctive features of the primate genome is the Alu element, a repetitive short interspersed element, over a million highly similar copies of which account for 〉10% of the genome. A direct consequence of this feature is that primates' transcriptome is highly enriched in long stable dsRNA structures, the preferred target of adenosine deaminases acting on RNAs (ADARs), which are the enzymes catalyzing A-to-I RNA editing. Indeed, A-to-I editing by ADARs is extremely abundant in primates: over a hundred million editing sites exist in their genomes. However, there are few essential editing sites conserved across mammals that have maintained their editing level despite the radical change in ADAR target landscape. Here, we review and discuss the cost of having an unusual amount of dsRNA and editing in the transcriptome, as well as the opportunities it presents, which might have contributed to the accelerated evolution of the primates. Invasion of Alu repeats into the primate genome created a plethora of new A-to-I RNA editing targets. How can the editing machinery maintain regulation of editing levels in the few essential sites in face of the drastic change in the editome landscape? Has necessity to overcome this challenge led to innovative functional editing in the course of primate evolution?
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    Multi-tasking of biosynthetic and energetic functions of glycolysis explained by supply and demand logic (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-10-29
    Description: After more than a century of research on glycolysis, we have detailed descriptions of its molecular organization, but despite this wealth of knowledge, linking the enzyme properties to metabolic pathway behavior remains challenging. These challenges arise from multi-layered regulation and the context and time dependence of component functions. However, when viewed as a system that functions according to the principles of supply and demand, a simplifying theoretical framework can be applied to study its regulation logic and to assess the coherence of experimental interpretations. These principles are universally applicable, as they emphasize the common metabolic tasks of glycolysis: the provision of free-energy carriers, and precursors for biosynthesis and stress-related compounds. Here we will review the regulation of multi-tasking by glycolysis and consider how an understanding of this central metabolic pathway can be pursued using general principles, rather than focusing on the biochemical details of constituent components. An intuitive understanding of multi-tasking by glycolysis is complicated by many interactions and dynamic, multi-layered regulation. Viewed as a system that functions according to the principles of supply and demand, a simplifying theoretical framework can be applied to study its regulation logic and to assess the coherence of experimental interpretations.
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    UvrD helicase: An old dog with a new trick (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-10-28
    Description: Transcription-coupled repair (TCR) is a phenomenon that exists in a wide variety of organisms from bacteria to humans. This mechanism allows cells to repair the actively transcribed DNA strand much faster than the non-transcribed one. At the sites of bulky DNA damage RNA polymerase stalls, initiating recruitment of the repair machinery. It is a commonly accepted paradigm that bacterial cells utilize a sole coupling factor, called Mfd to initiate TCR. According to that model, Mfd removes transcription complexes stalled at the lesion site and simultaneously recruits repair machinery. However, this model was recently put in doubt by various discrepancies between the proposed universal role of Mfd in the TCR and its biochemical and phenotypical properties. Here, I present a second pathway of bacterial TCR recently discovered in my laboratory, which does not involve Mfd but implicates a common repair factor, UvrD, in a central position in the process. Two pathways of transcription-coupled repair. Left: During acute stress RNAP stalled at a lesion is pushed back by UvrD without transcript loss and after repair by the NER machinery transcription resumes. Right: At steady-state level of DNA damage stalled RNAP is pushed forward by Mfd, which displaces RNA polymerase to allow the repair.
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    Closing the genotype–phenotype gap: Emerging technologies for evolutionary genetics in ecological model vertebrate systems (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-11-08
    Description: The analysis of genetic and epigenetic mechanisms of the genotype–phenotypic connection has, so far, only been possible in a handful of genetic model systems. Recent technological advances, including next-generation sequencing methods such as RNA-seq, ChIP-seq and RAD-seq, and genome-editing approaches including CRISPR-Cas, now permit to address these fundamental questions of biology also in organisms that have been studied in their natural habitats. We provide an overview of the benefits and drawbacks of these novel techniques and experimental approaches that can now be applied to ecological and evolutionary vertebrate models such as sticklebacks and cichlid fish. We can anticipate that these new methods will increase the understanding of the genetic and epigenetic factors influencing adaptations and phenotypic variation in ecological settings. These new arrows in the methodological quiver of ecologist will drastically increase the understanding of the genetic basis of adaptive traits – leading to a further closing of the genotype–phenotype gap. Novel methods are currently revolutionizing the fields of ecology and evolutionary biology. They facilitate the investigation of genotype–phenotype-associations and permit the analysis of cis-regulatory and epigenetic underpinnings of adaptive traits. For the first time transgenesis and genome-editing tools allow the validation of targets in ecological model organisms.
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    On a matter of seminal importance (2014)
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    In: BioEssays
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    Publication Date: 2014-11-08
    Description: Egg and sperm have, understandably, been the “stars” of mammalian fertilization biology, particularly because artificial reproductive technologies allow for fertilization to occur outside of the female reproductive tract without other apparent contributions from either sex. Yet, recent research, including an exciting new paper, reveals unexpected and important contributions of seminal plasma to fertility. For example, seminal plasma proteins play critical roles in modulating female reproductive physiology, and a new study in mice demonstrates that effects of some of these proteins on the female can even affect the health of her progeny. Furthermore, although several actions of seminal plasma have been conserved across taxa, male accessory glands and their products are diverse – even among mammals. Taken together, these studies suggest that the actions of seminal plasma components are important to understand, and also to consider in future development of assisted reproductive technologies (ART) for humans, farm species and endangered species of mammals. Although eggs and sperm can combine to generate embryos (upper equation), studies in a range of organisms show that seminal plasma components (stars, in the lower equation) enhance fertility by modulating the physiology of the female and – based on a recent study – improving the health of her progeny. The sperm diagram is based on a photo of a human sperm in Smith et al. (2009, Cell Motil. Cytoskel . 66 : 220–36). The very happy emoticon in the lower equation is from: http://www.graphicsfuel.com/2012/09/happy-and-sad-emoticons-psd/ .
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    A reverse gear for transcription-coupled DNA repair? (Comment on DOI 10.1002/bies.201400106) (2014)
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    In: BioEssays
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    Publication Date: 2014-11-08
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    BioEssays 12∕2014 (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-11-11
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    BioEssays 12∕2014 (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-11-11
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    Getting what you paid for in quality control? Cell lines exemplify a more general challenge (2014)
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    In: BioEssays
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    Publication Date: 2014-11-11
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    Genomics approaches to study musical aptitude (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-08-27
    Description: Although music and other forms of art can develop in diverse directions, they are linked to the genetic profiles of populations. Hearing music is a strong environmental trigger that serves as an excellent model to study the crosstalk between genes and the environment. We propose that the ability to enjoy and practice music requires musical aptitude, which is a common and innate trait facilitating the enjoyment and practice of music. The innate drive for music can only have arisen by exposure to music, and it develops with motivation and training in musically rich environments. Recent genomic approaches have shown that the genes responsible for inner ear development, auditory pathways and neurocognitive processes may underlay musical aptitude. It is expected that genomic approaches can be applied to musical traits and will reveal new biological mechanisms that affect human evolution, brain function, and civilisation. Can genes explain why some people are more interested in music than others? Genomics approaches enable to study the biological background of musical aptitude in an unbiased, hypothesis-free fashion, without any prior knowledge about the biological background. Genome-wide analyses of musical aptitude identified candidate genes that affect the auditory pathway and neurocognitive functions.
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    Experimental evidence needed to demonstrate inter- and trans-generational effects of ancestral experiences in mammals (2014)
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    In: BioEssays
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    Publication Date: 2014-08-27
    Description: Environmental factors routinely influence an organism's biology. The inheritance or transmission of such influences to descendant generations would be an efficient mode of information transfer across generations. The developmental stage at which a specific environment is encountered by the ancestral generation, and the number of generations over which information about that environment is registered, determines an inter- vs. trans-generational effect of ancestral influence. This commentary will outline the distinction between these influences. While seductive in principle, inter- and trans-generational inheritance in mammals is a hotly debated area of research inquiry. We present constructive criticism of such inheritance, and suggest potential experimental avenues for reconciliation. Finally, epigenetic mechanisms present an avenue for gene regulation that is dynamic. We briefly discuss how such malleability affords the potential for a reversal of any detrimental environmental influences that might have adversely impacted ancestral or descendant generations. Influence of ancestral environments on descendant biology are accumulating. It is important to distinguish these influences as inter- or trans-generational inheritance. Questions remain about how gametes are marked by ancestral environmental factors, and how genetic loci that are marked by epigenetic mechanisms escape from epigenetic reprogramming.
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    How discordant morphological and molecular evolution among microorganisms can revise our notions of biodiversity on Earth (2014)
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    In: BioEssays
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    Publication Date: 2014-08-27
    Description: Microscopy has revealed tremendous diversity of bacterial and eukaryotic forms. Recent molecular analyses show discordance in estimates of biodiversity between morphological and molecular analyses. Moreover, phylogenetic analyses of the diversity of microbial forms reveal evidence of convergence at scales as deep as interdomain: morphologies shared between bacteria and eukaryotes. Here, we highlight examples of such discordance, focusing on exemplary lineages such as testate amoebae, ciliates, and cyanobacteria. These have long histories of morphological study, enabling deeper analyses on both the molecular and morphological sides. We discuss examples in two main categories: (i) morphologically identical (or highly similar) individuals that are genetically distinct and (ii) morphologically distinct individuals that are genetically the same. We argue that hypotheses about discordance can be tested using the concept of neutral morphologies, or more broadly neutral phenotypes, as a null hypothesis. Recent phylogenies of microbial lineages, combined with microscopical studies, reveal instances of discordance between molecular and morphological evolution. Here, we focus on exemplary microbial lineages with long histories of morphological study. We propose that instances of discordance can be tested using the concept of neutral morphologies as a null hypothesis.
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    Cracking the ANP32 whips: Important functions, unequal requirement, and hints at disease implications (2014)
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    In: BioEssays
    Details
    Publication Date: 2014-08-27
    Description: The acidic (leucine-rich) nuclear phosphoprotein 32 kDa (ANP32) family is composed of small, evolutionarily conserved proteins characterized by an N-terminal leucine-rich repeat domain and a C-terminal low-complexity acidic region. The mammalian family members (ANP32A, ANP32B, and ANP32E) are ascribed physiologically diverse functions including chromatin modification and remodelling, apoptotic caspase modulation, protein phosphatase inhibition, as well as regulation of intracellular transport. In addition to reviewing the widespread literature on the topic, we present a concept of the ANP32s as having a whip-like structure. We also present hypotheses that ANP32C and other intronless sequences should not currently be considered bona fide family members, that their disparate necessity in development may be due to compensatory mechanisms, that their contrasting roles in cancer are likely context-dependent, along with an underlying hypothesis that ANP32s represent an important node of physiological regulation by virtue of their diverse biochemical activities. This essay surveys our understanding of the ANP32 proteins, a family of multifunctional factors conserved in most eukaryotes. Based primarily on studies of mammalian ANP32A, ANP32B, and ANP32E, we hypothesize that these regulators of chromatin, caspases, phosphatases, and mRNA transport coordinate disparate pathways and potentially impact disease states.
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    Lysine methylation in cancer: SMYD3-MAP3K2 teaches us new lessons in the Ras-ERK pathway (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-09-03
    Description: Lysine methylation has been traditionally associated with histones and epigenetics. Recently, lysine methyltransferases and demethylases – which are involved in methylation of non-histone substrates – have been frequently found deregulated in human tumours. In this realm, a new discovery has unveiled the methyltransferase SMYD3 as an enhancer of Ras-driven cancer. SMYD3 is up-regulated in different types of tumours. SMYD3-mediated methylation of MAP3K2 increases mutant K-Ras-induced activation of ERK1/2. Methylation of MAP3K2 prevents it from binding to the phosphatase PP2A, thereby impeding the impact of this negative regulator on Ras-ERK1/2 signals, leading to the formation of lung and pancreatic adenocarcinomas. Furthermore, depletion of SMYD3 synergises with a MEK inhibitor, currently in clinical trials, to block Ras-driven pancreatic neoplasia. These results underscore the importance of lysine methylation in the regulation of signalling pathways relevant for tumourigenesis and endorse the development of drugs targeting unregulated lysine methylation as therapeutic agents in the struggle against cancer. Lysine methylation is traditionally associated with histones and epigenetics. Recently, lysine methyltransferases involved in methylation of non-histone substrates have been frequently found deregulated in tumours. Now methyltransferase SMYD3 has been identified as an enhancer of Ras-driven cancer via methylation of MAP3K2, which prevents it from binding to the phosphatase PP2A, thereby mitigating its negative regulation of Ras-ERK1/2 signals, hence promoting tumourigenesis.
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    Pre-birth world and the development of the immune system: Mum's diet affects our adult health (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-09-03
    Description: Secondary lymphoid organs form in utero through an inherited and well-established developmental program. However, maternal non-heritable features can have a major impact on the gene expression of the embryo, hence influencing the future health of the offspring. Recently, maternal retinoids were shown to regulate the formation of immune structures, shedding light on the role of maternal nutrition in the genetic signature of emergent immune cells. Here we highlight evidence showing how the maternal diet influences the establishment of the immune system, and we also discuss how unbalanced maternal diets may set the response to infection and vaccination in the progeny. Maternal nutrition has a major impact on the developing immune system, hence influencing the future health of the progeny. Recent findings revealed that retinoic acid, derived from the maternal diet intake of vitamin A, is critical for the development of secondary lymphoid organs in the embryo, such as lymph nodes and Peyer's patches, which in turn pre-set the efficiency of adaptive immune responses throughout life.
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    How does oncogene transformation render tumor cells hypersensitive to nutrient deprivation? (2014)
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    In: BioEssays
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    Publication Date: 2014-09-23
    Description: Oncogene activation leads to cellular transformation by deregulation of biological processes such as proliferation and metabolism. Paradoxically, this can also sensitize cells to nutrient deprivation, potentially representing an Achilles' heel in early stage tumors. The mechanisms underlying this phenotype include loss of energetic and redox homeostasis as a result of metabolic reprogramming, favoring synthesis of macromolecules. Moreover, an emerging mechanism involving the deregulation of mRNA translation elongation through inhibition of eukaryotic elongation factor 2 kinase (eEF2K) is presented. The potential consequences of eEF2K deregulation leading to cell death under nutrient depletion are discussed. Finally, the relevance of eEF2K as a master regulator of the response to nutrient deprivation in vivo, and its potential exploitation for therapeutic targeting of cancers, are elaborated. Overall, a better understanding of the adaptive mechanisms allowing tumors to circumvent oncogene-induced hypersensitivity to nutrient deprivation is a promising avenue for uncovering novel therapeutic targets in cancers. Oncogene activation leads to hypersensitivity to nutrient deprivation by deregulation of specific metabolic pathways. Novel mechanisms underlying this phenotype are emerging, such as altered control of mRNA translation elongation by inhibition of the eEF2 kinase (eEF2K). The adaptive mechanisms used to circumvent oncogene-mediated cell death under nutrient deprivation are described.
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    Incorporating alternative splicing and mRNA editing into the genetic analysis of complex traits (2014)
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    In: BioEssays
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    Publication Date: 2014-08-30
    Description: The nomination of candidate genes underlying complex traits is often focused on genetic variations that alter mRNA abundance or result in non-conservative changes in amino acids. Although inconspicuous in complex trait analysis, genetic variants that affect splicing or RNA editing can also generate proteomic diversity and impact genetic traits. Indeed, it is known that splicing and RNA editing modulate several traits in humans and model organisms. Using high-throughput RNA sequencing (RNA-seq) analysis, it is now possible to integrate the genetics of transcript abundance, alternative splicing (AS) and editing with the analysis of complex traits. We recently demonstrated that both AS and mRNA editing are modulated by genetic and environmental factors, and potentially engender phenotypic diversity in a genetically segregating mouse population. Therefore, the analysis of splicing and RNA editing can expand not only the regulatory landscape of transcriptome and proteome complexity, but also the repertoire of candidate genes for complex traits. The complex molecular mechanisms that modulate the relationship between genetic variations and quantitative traits are often depicted in broad cellular transcriptional networks. Therefore, a comprehensive genetic analysis of the cellular transcript abundance, levels of alternative splicing, and RNA editing, will help to delineate the mechanisms that modulate the genotype-phenotype relationship.
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    Replication protein A: Single-stranded DNA's first responder (2014)
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    In: BioEssays
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    Publication Date: 2014-08-30
    Description: Replication protein A (RPA), the major single-stranded DNA-binding protein in eukaryotic cells, is required for processing of single-stranded DNA (ssDNA) intermediates found in replication, repair, and recombination. Recent studies have shown that RPA binding to ssDNA is highly dynamic and that more than high-affinity binding is needed for function. Analysis of DNA binding mutants identified forms of RPA with reduced affinity for ssDNA that are fully active, and other mutants with higher affinity that are inactive. Single molecule studies showed that while RPA binds ssDNA with high affinity, the RPA complex can rapidly diffuse along ssDNA and be displaced by other proteins that act on ssDNA. Finally, dynamic DNA binding allows RPA to prevent error-prone repair of double-stranded breaks and promote error-free repair. Together, these findings suggest a new paradigm where RPA acts as a first responder at sites with ssDNA, thereby actively coordinating DNA repair and DNA synthesis. Replication protein A (RPA) binds single-strand DNA intermediates in DNA replication, repair, and recombination. Recent studies have demonstrated that RPA-DNA interactions are highly dynamic and suggest that this dynamism contributes to the functions of RPA and is necessary for genome stability.
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    Single-molecule pull-down (SiMPull) for new-age biochemistry (2014)
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    In: BioEssays
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    Publication Date: 2014-08-30
    Description: Macromolecular interactions play a central role in many biological processes. Protein-protein interactions have mostly been studied by co-immunoprecipitation, which cannot provide quantitative information on all possible molecular connections present in the complex. We will review a new approach that allows cellular proteins and biomolecular complexes to be studied in real-time at the single-molecule level. This technique is called single-molecule pull-down (SiMPull), because it integrates principles of conventional immunoprecipitation with the powerful single-molecule fluorescence microscopy. SiMPull is used to count how many of each protein is present in the physiological complexes found in cytosol and membranes. Concurrently, it serves as a single-molecule biochemical tool to perform functional studies on the pulled-down proteins. In this review, we will focus on the detailed methodology of SiMPull, its salient features and a wide range of biological applications in comparison with other biosensing tools. A recent single-molecule pull-down method (SiMPull) has been described in detail, which enables determination of absolute copy number of protein complexes, the stoichiometry of each protein in the complex and their functional properties all in matter of minutes directly from whole cell or tissue extracts.
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    LRRC8s revisited: And now they SWELL! (Retrospective on DOI 10.1002/bies.201100173) (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-09-26
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    Review of Arrival of the fittest: Solving evolution's greatest puzzle (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-09-26
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    Regenerative versus destructive cell death in developing systems and tissue homeostasis (retrospective on DOI 10.1002/bies.201200018) (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-09-26
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    Mutational heterogeneity: A key ingredient of bet-hedging and evolutionary divergence? (2014)
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    In: BioEssays
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    Publication Date: 2014-11-06
    Description: Here, we propose that the heterogeneity of mutational types in populations underpins alternative pathways of evolutionary adaptation. Point mutations, deletions, insertions, transpositions and duplications cause different biological effects and provide distinct adaptive possibilities. Experimental evidence for this notion comes from the mutational origins of adaptive radiations in large, clonal bacterial populations. Independent sympatric lineages with different phenotypes arise from distinct genetic events including gene duplication, different insertion sequence movements and several independent point mutations. The breadth of the mutational spectrum in the ancestral population should be viewed as a form of bet-hedging, reducing the risk of evolutionary dead ends and complementing the phenotypic and epigenetic heterogeneities that improve the survival capabilities of a population. Different mutational events arise from distinct cellular processes and are subject to separate environmental impacts, so the availability of any particular type of mutation may constrain or promote adaptive pathways in populations. Distinct types of mutation have different phenotypic effects. Sub-populations containing different mutations provide alternative starting points for adaptation and originate parallel lines of evolution, initiating sympatric divergence. The mutational heterogeneity can be viewed as a form of bet-hedging, initiating alternative evolutionary solutions that have different risks associated with them.
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    The emerging functions of oligodendrocytes in regulating neuronal network behaviour (2014)
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    In: BioEssays
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    Publication Date: 2014-11-05
    Description: Myelin is required for efficient nerve conduction, but not all axons are myelinated to the same extent. Here we review recent studies that have revealed distinct myelination patterns of different axonal paths, suggesting that myelination is not an all or none phenomenon and that its presence is finely regulated in central nervous system networks. Whereas powerful reductionist biology has led to important knowledge of how oligodendrocytes function by themselves, little is known about their role in neuronal networks. We still do not understand how oligodendrocytes integrate information from neurons to adapt their function to the need of the system. An intricate cross talk between neurons and glia is likely to exist and to determine how neuronal circuits operate as a whole. Dissecting these mechanisms by using integrative systems biology approaches is one of the major challenges ahead. Beyond the role of myelin in speeding up nerve conduction, its function in the fine-tuning of neuronal networks is just emerging. This new concept of myelin plasticity implies that oligodendrocytes are able to sense neuronal activity and adapt myelination, resulting in a wider range of consequences than previously thought.
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    No ECSIT-stential evidence for a link with Alzheimer's disease yet (retrospective on DOI 10.1002/bies.201100193) (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-11-05
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    E-cadherin's role in development, tissue homeostasis and disease: Insights from mouse models (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-12-03
    Description: Recent studies uncovered critical roles of the adhesion protein E-cadherin in health and disease. Global inactivation of Cdh1 , the gene encoding E-cadherin in mice, results in early embryonic lethality due to an inability to form the trophectodermal epithelium. To unravel E-cadherin's functions beyond development, numerous mouse lines with tissue-specific disruption of Cdh1 have been generated. The consequences of E-cadherin loss showed great variability depending on the tissue in question, ranging from nearly undetectable changes to a complete loss of tissue structure and function. This review focuses on these studies and discusses how they provided important insights into E-cadherin's role in cell adhesion, proliferation and differentiation, and its consequences for biological processes as epithelial-to-mesenchymal transition, vascularization, and carcinogenesis. Lastly, we present some perspectives and possible approaches for future research. E-cadherin is a cell adhesion protein with critical roles in development, tissue homeostasis, and disease. We focus on mouse lines with organ-specific E-cadherin disruption and the insights they provided into E-cadherin's role in cell adhesion, proliferation and differentiation, epithelial-to-mesenchymal transition, vascularization, and carcinogenesis.
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    Paracrine signaling mediated at cell–cell contacts (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-12-06
    Description: Recent findings in several organ systems show that cytoneme-mediated signaling transports signaling proteins along cellular extensions and targets cell-to-cell exchanges to synaptic contacts. This mechanism of paracrine signaling may be a general one that is used by many (or all) cell types in many (or all) organs. We briefly review these findings in this perspective. We also describe the properties of several signaling systems that have previously been interpreted to support a passive diffusion mechanism of signaling protein dispersion, but can now be understood in the context of the cytoneme mechanism. Also watch the Video Abstract . The importance of paracrine signaling for animal development has been recognized for almost 100 years, but the discovery that epithelial cells transport signaling proteins over long distances with filopodia that make direct contact with target cells is recent. In this perspective we review the new findings and explore some of their many implications.
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    How do environmental factors influence life cycles and development? An experimental framework for early-diverging metazoans (2014)
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    In: BioEssays
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    Publication Date: 2014-09-11
    Description: Ecological developmental biology (eco-devo) explores the mechanistic relationships between the processes of individual development and environmental factors. Recent studies imply that some of these relationships have deep evolutionary origins, and may even pre-date the divergences of the simplest extant animals, including cnidarians and sponges. Development of these early diverging metazoans is often sensitive to environmental factors, and these interactions occur in the context of conserved signaling pathways and mechanisms of tissue homeostasis whose detailed molecular logic remain elusive. Efficient methods for transgenesis in cnidarians together with the ease of experimental manipulation in cnidarians and sponges make them ideal models for understanding causal relationships between environmental factors and developmental mechanisms. Here, we identify major questions at the interface between animal evolution and development and outline a road map for research aimed at identifying the mechanisms that link environmental factors to developmental mechanisms in early diverging metazoans. Also watch the Video Abstract . Understanding the diversity of genome-environment interactions requires integrative, multidisciplinary, and modeling-based approaches. Representative cnidarians and sponges provide novel opportunities to investigate how the environment interacts with developmental processes and, in turn, how developmental evolution affects the environment.
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    BioEssays 10∕2014 (2014)
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    In: BioEssays
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    Publication Date: 2014-09-11
    Description: Take it up . It was recently shown that horizontal gene transfer (HGT) not only takes place in the form of long DNA fragments, but that it may also occur with short and damaged DNA (down to 20 bp in length). The integration of these short fragments is achieved at replication forks, and this process opens up the possibility for genetic exchange across distinct species in both time and space. On pages 1005–1010 of this issue, Søren Overballe-Petersen and Eske Willerslev further elaborate on their findings and speculate on the potential evolutionary consequences of this phenomenon. Cover by Søren Overballe-Petersen and Eske Willerslev.
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    BioEssays 10∕2014 (2014)
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    In: BioEssays
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    Publication Date: 2014-09-11
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    At the mercy of our microbes? (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-09-11
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    BioEssays 10∕2014 (2014)
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    In: BioEssays
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    Publication Date: 2014-09-11
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    BioEssays – Next Issue (2014)
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    Publication Date: 2014-09-11
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    Forces shaping the antibiotic resistome (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-09-12
    Description: Antibiotic resistance has become a problem of global scale. Resistance arises through mutation or through the acquisition of resistance gene(s) from other bacteria in a process called horizontal gene transfer (HGT). While HGT is recognized as an important factor in the dissemination of resistance genes in clinical pathogens, its role in the environment has been called into question by a recent study published in Nature . The authors found little evidence of HGT in soil using a culture-independent functional metagenomics approach, which is in contrast to previous work from the same lab showing HGT between the environment and human microbiome. While surprising at face value, these results may be explained by the lack of selective pressure in the environment studied. Importantly, this work suggests the need for careful monitoring of environmental antibiotic pollution and stringent antibiotic stewardship in the fight against resistance. Inter-environment horizontal gene transfer (HGT) (gray arrows) is frequent, while intra-environmental HGT is less frequent (black arrows). Antibiotic selection may increase HGT and/or gene fixation (larger arrows), while genetic drift may decrease HGT in the environment (smaller arrows). Monitoring and control of antibiotic use and pollution is of paramount importance.
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    Experience and the ever-changing brain: What the transcriptome can reveal (2014)
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    In: BioEssays
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    Publication Date: 2014-09-12
    Description: The brain is an ever-changing organ that encodes memories and directs behavior. Neuroanatomical studies have revealed structural plasticity of neural architecture, and advances in gene expression technology and epigenetics have demonstrated new mechanisms underlying the brain's dynamic nature. Stressful experiences challenge the plasticity of the brain, and prolonged exposure to environmental stress redefines the normative transcriptional profile of both neurons and glia, and can lead to the onset of mental illness. A more thorough understanding of normal and abnormal gene expression is needed to define the diseased brain and improve current treatments for psychiatric disorders. The efforts to describe gene expression networks have been bolstered by microarray and RNA-sequencing technologies. The heterogeneity of neural cell populations and their unique microenvironments, coupled with broad ranging interconnectivity, makes resolving this complexity exceedingly challenging and requires the combined efforts of single cell and systems level expression profiling to identify targets for therapeutic intervention. Transcriptional profiling techniques are revealing novel mechanisms underlying stress-induced neuroplasticity and yielding new insights into mood disorders. The image illustrates how the same stressor produces unique transcriptional profiles depending on the stress history of the mouse, highlighting how past experiences can alter cellular reactivity in certain dynamic brain regions.
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    ATP puts the brake on DNA double-strand break repair (2014)
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    In: BioEssays
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    Publication Date: 2014-09-12
    Description: DNA double-strand breaks (DSBs) are one of the most deleterious forms of DNA damage and can result in cell inviability or chromosomal aberrations. The Mre11-Rad50-Nbs1 (MRN) ATPase-nuclease complex is a central player in the cellular response to DSBs and is implicated in the sensing and nucleolytic processing of DSBs, as well as in DSB signaling by activating the cell cycle checkpoint kinase ATM. ATP binding to Rad50 switches MRN from an open state with exposed Mre11 nuclease sites to a closed state with partially buried nuclease sites. The functional meaning of this switch remained unclear. A new study shows that ATP binding to Rad50 promotes DSB recognition, tethering, and ATM activation, while ATP hydrolysis opens the nuclease active sites to promote processing of DSBs. MRN thus emerges as functional switch that may coordinate the temporal transition from signaling to processing of DSBs. The Mre11-Rad50-Nbs1 (MRN) complex is a key factor in the tethering, damage signaling, and processing of DNA ends in DNA double-strand break (DSB) repair. A recent study identifies MRN as a functional switch, where ATP switches MRN between DSB signaling/tethering and DNA processing modes.
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    Microbial gardening in the ocean's twilight zone: Detritivorous metazoans benefit from fragmenting, rather than ingesting, sinking detritus (2014)
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    In: BioEssays
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    Publication Date: 2014-09-13
    Description: Sinking organic particles transfer ∼10 gigatonnes of carbon into the deep ocean each year, keeping the atmospheric CO 2 concentration significantly lower than would otherwise be the case. The exact size of this effect is strongly influenced by biological activity in the ocean's twilight zone (∼50–1,000 m beneath the surface). Recent work suggests that the resident zooplankton fragment, rather than ingest, the majority of encountered organic particles, thereby stimulating bacterial proliferation and the deep-ocean microbial food web. Here we speculate that this apparently counterintuitive behaviour is an example of ‘microbial gardening’, a strategy that exploits the enzymatic and biosynthetic capabilities of microorganisms to facilitate the ‘gardener's’ access to a suite of otherwise unavailable compounds that are essential for metazoan life. We demonstrate the potential gains that zooplankton stand to make from microbial gardening using a simple steady state model, and we suggest avenues for future research. Zooplankton in the ocean's twilight zone typically consume nutritionally poor detritus. We speculate that these animals fragment large detrital particles to stimulate the growth of microorganisms. This ‘gardening’ of microbes exploits their enzymatic and biosynthetic pathways to produce biomass that can be harvested as an energy-rich and nutritious food source.
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    Unique features of DNA replication in mitochondria: A functional and evolutionary perspective (2014)
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    In: BioEssays
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    Publication Date: 2014-09-13
    Description: Last year, we reported a new mechanism of DNA replication in mammals. It occurs inside mitochondria and entails the use of processed transcripts, termed bootlaces, which hybridize with the displaced parental strand as the replication fork advances. Here we discuss possible reasons why such an unusual mechanism of DNA replication might have evolved. The bootlace mechanism can minimize the occurrence and impact of single-strand breaks that would otherwise threaten genome stability. Furthermore, by providing an implicit mismatch recognition system, it should limit the occurrence of replication-dependent deletions and insertions, and defend against invading elements. Such a mechanism may also limit attempts to manipulate the mammalian mitochondrial genome. Short pieces of RNA serve as precursors to DNA replication in many systems, but the long RNAs hybridized to replicating DNA in mitochondria are unusual if not unique. Here we discuss the virtues of threading RNA transcripts (aka bootlaces) onto the lagging-strand template, rather than the conventional approach of synthesizing DNA concurrently on both strands.
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    Now you see it: Genome methylation makes a comeback in Drosophila (2014)
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    In: BioEssays
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    Publication Date: 2014-09-13
    Description: Drosophila melanogaster is often considered to lack genomic 5-methylcytosine (m 5 C), an opinion reinforced by two whole genome bisulfite-sequencing studies that failed to find m 5 C. New evidence, however, indicates that genomic methylation is indeed present in the fly, albeit in small quantities and in unusual patterns. At embryonic stage 5, m 5 C occurs in short strand-specific regions that cover ∼1% of the genome, at tissue levels suggesting a distribution restricted to a subset of nuclei. Its function is not obvious, but methylation in subsets of nuclei would obscure functional associations since transcript levels and epigenetic modifications are assayed in whole embryos. Surprisingly, Mt2, the fly's only candidate DNA methyltransferase, is not necessary for the observed methylation. Full evaluation of the functions of genome methylation in Drosophila must await discovery and experimental inactivation of the DNA methyltransferase, as well as a better understanding of the pattern and developmental regulation of genomic m 5 C. Methylcytosine immunoprecipitation and deep sequencing reveal a strand-asymmetric pattern of cytosine methylation in the fly genome (top). Short regions (middle) contain methylcytosine in non-CpG sequence motifs (bottom). The regions are methylated in only a fraction of fly genomes; specific regions might be methylated in distinct subsets of embryonic nuclei (right).
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    How cells explore shape space: A quantitative statistical perspective of cellular morphogenesis (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-09-13
    Description: Through statistical analysis of datasets describing single cell shape following systematic gene depletion, we have found that the morphological landscapes explored by cells are composed of a small number of attractor states. We propose that the topology of these landscapes is in large part determined by cell-intrinsic factors, such as biophysical constraints on cytoskeletal organization, and reflects different stable signaling and/or transcriptional states. Cell-extrinsic factors act to determine how cells explore these landscapes, and the topology of the landscapes themselves. Informational stimuli primarily drive transitions between stable states by engaging signaling networks, while mechanical stimuli tune, or even radically alter, the topology of these landscapes. As environments fluctuate, the topology of morphological landscapes explored by cells dynamically adapts to these fluctuations. Finally we hypothesize how complex cellular and tissue morphologies can be generated from a limited number of simple cell shapes. Morphological landscape generated by statistical analysis of cell shape following systematic RNA interference. The landscape is derived such that the central peak of the landscape represents the most frequent or “normal” (N shape). Changes in signaling state result in cells being drawn into different attractors (L, C, T, R shapes).
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    A chromosome separation checkpoint (2014)
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    In: BioEssays
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    Publication Date: 2014-12-04
    Description: Here we discuss a “chromosome separation checkpoint” that might regulate the anaphase-telophase transition. The concept of cell cycle checkpoints was originally proposed to account for extrinsic control mechanisms that ensure the order of cell cycle events. Several checkpoints have been shown to regulate major cell cycle transitions, namely at G1-S and G2-M. At the onset of mitosis, the prophase-prometaphase transition is controlled by several potential checkpoints, including the antephase checkpoint, while the spindle assembly checkpoint guards the metaphase-anaphase transition. Our hypothesis is based on the recently uncovered feedback control mechanism that delays chromosome decondensation and nuclear envelope reassembly until effective separation of sister chromatids during anaphase is achieved. A central player in this potential checkpoint is the establishment of a constitutive, midzone-based Aurora B phosphorylation gradient that monitors the position of chromosomes along the spindle axis. We propose that this surveillance mechanism represents an additional step towards ensuring mitotic fidelity. A chromosome separation checkpoint delays chromosome decondensation and nuclear envelope reassembly until effective separation of sister chromatids during anaphase is achieved. A midzone-based Aurora B phosphorylation gradient monitors the position of chromosomes along the spindle axis. We propose that this surveillance mechanism represents an additional step towards ensuring mitotic fidelity.
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    BioEssays 1∕2015 (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-12-18
    Description: Histone Proteolysis: A proposal for categorization into ‘Clipping’ and ‘Degradation’ . On pages 70–79 of this issue, Dhaenens et al. try to cast a new light onto the black box of 40 years of incoherent reports on histone proteolysis. The difficulties of specifying the in vivo versus in vitro origin of this post-translational modification, the fact that the same enzymes mediate both “histone degradation” and the epigenetically connoted “histone clipping”, and the complexity and redundancy of the histone code, all contribute to the surprising shortage of reports on the biology of this potentially far-reaching posttranslational modification. Cover design: Tim De Vocht (based on artwork from David S. Goodsell).
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    Inside the cell: One of a series, but something special … (2014)
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    In: BioEssays
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    Publication Date: 2014-12-18
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    BioEssays 1∕2015 (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-12-18
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    A century of phage research: Bacteriophages and the shaping of modern biology (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-12-18
    Description: 2015 marks the centennial of the discovery of bacteriophages, viruses that infect bacteria. Phages have been central to some of biology's most meaningful advances over the past hundred years (shown here); they greatly influence the workings of the biosphere, and are poised to play expanded roles in biomedicine, biotechnology, and ecology.
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    BioEssays – Next Issue (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-12-18
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    Maternal histone variants and their chaperones promote paternal genome activation and boost somatic cell reprogramming (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-10-19
    Description: The mammalian egg employs a wide spectrum of epigenome modification machinery to reprogram the sperm nucleus shortly after fertilization. This event is required for transcriptional activation of the paternal/zygotic genome and progression through cleavage divisions. Reprogramming of paternal nuclei requires replacement of sperm protamines with canonical and non-canonical histones, covalent modification of histone tails, and chemical modification of DNA (notably oxidative demethylation of methylated cytosines). In this essay we highlight the role maternal histone variants play during developmental reprogramming following fertilization. We discuss how reduced maternal histone variant incorporation in somatic nuclear transfer experiments may explain the reduced viability of resulting embryos and how knowledge of repressive and activating maternal factors may be used to improve somatic cell reprogramming. During fertilization, newly synthesized histones from the oocyte are deposited onto the paternal genome (replacing protamines) and facilitate paternal genomic reprogramming. Recently, Shinagawa and colleagues have found that some of these same maternal histone variants can facilitate somatic cell reprogramming in combination with their corresponding chaperones.
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    The shades of gray of the chromatin fiber (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-10-19
    Description: The chromatin fiber consists of a string of nucleosomes connected by linker DNA regions. The hierarchy of folding of this fiber within the cell has long been controversial, and the existence of an originally described 30 nm fiber has been debated and reviewed extensively. This review contextualizes two recent papers on this topic that suggest the 30 nm fiber to be an over-simplification. The idealized model from the first study provides good insight into the constraints and histone participation in the maintenance of the fiber structure. The second paper provides a theoretical description of a more realistic view of the highly heterogeneous and dynamic chromatin organization in the in vivo setting. It is now time to abandon the highly regular “one start” solenoidal 30 nm structure and replace it with a more realistic highly dynamic, polymorphic fiber. The chromatin fiber consists of a string of nucleosomes connected by linker DNA regions. Over the years, its structure has long been controversial. Two recent papers provide key insights into the folding constraints and histone participation and to a more realistic view of its heterogeneous and dynamic organization.
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    Do age-associated DNA methylation changes increase the risk of malignant transformation? (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-10-11
    Description: Aging of the organism is associated with highly reproducible DNA methylation (DNAm) changes, which facilitate estimation of donor age. Cancer is also associated with DNAm changes, which may contribute to disease development. Here, we speculate that age-associated DNAm changes may increase the risk of tumor initiation. Notably, when using epigenetic signatures for age-estimations tumor cells are often predicted to be much older than the chronological age of the patient. We demonstrate that aberrant hypermethylation within the gene DNA methyltransferase 3A ( DNMT3A ) – which may contribute to initiation of acute myeloid leukemia (AML) – is particularly observed in AML samples that reveal significantly more age-associated DNAm changes. The functional relevance of age-associated DNAm changes remains to be elucidated, but they occur genome wide, in a highly reproducible manner, and most likely influence chromatin organization – and hence may favor acquisition of aberrant DNAm patterns contributing to cancer in the elderly. Age-predictors based on specific DNA-methylation (DNAm) changes reflect biological aging. The global changes in DNAm pattern may also trigger aberrant DNAm – so called epimutations – that can initiate tumor formation in the elderly. The figure is adopted from Waddington's “epigenetic landscape” (The Strategy of The Genes. London, Allan & Unwin 1957).
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    BioEssays 11∕2014 (2014)
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    In: BioEssays
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    Publication Date: 2014-10-11
    Description: Maintaining genome stability during mitosis. On pages 1054–1061 Anthony Cesare discusses the cellular mechanisms that suppress double strand break repair (DSB) during mitosis. Suppressing this otherwise vital process during cell division seems to prevent the fusion of deprotected telomeres and therefore helps to maintain genomic integrity. Telomeres adopt three distinct protective states in relation to activation of the DNA damage response and DSB repair: closed-state, intermediate-state and uncapped-state telomeres. The cover depicts chromosomes with these different telomere states.
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    The world after print: Mind how you write, like never before… (2014)
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    In: BioEssays
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    Publication Date: 2014-10-11
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    BioEssays – Next Issue (2014)
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    In: BioEssays
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    Publication Date: 2014-10-11
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    BioEssays 11∕2014 (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-10-11
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    Why are most organelle genomes transmitted maternally? (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-10-11
    Description: Why the DNA-containing organelles, chloroplasts, and mitochondria, are inherited maternally is a long standing and unsolved question. However, recent years have seen a paradigm shift, in that the absoluteness of uniparental inheritance is increasingly questioned. Here, we review the field and propose a unifying model for organelle inheritance. We argue that the predominance of the maternal mode is a result of higher mutational load in the paternal gamete. Uniparental inheritance evolved from relaxed organelle inheritance patterns because it avoids the spread of selfish cytoplasmic elements. However, on evolutionary timescales, uniparentally inherited organelles are susceptible to mutational meltdown (Muller's ratchet). To prevent this, fall-back to relaxed inheritance patterns occurs, allowing low levels of sexual organelle recombination. Since sexual organelle recombination is insufficient to mitigate the effects of selfish cytoplasmic elements, various mechanisms for uniparental inheritance then evolve again independently. Organelle inheritance must therefore be seen as an evolutionary unstable trait, with a strong general bias to the uniparental, maternal, mode. Why chloroplasts and mitochondria are inherited maternally is a long standing and unsolved question. We propose that uniparental inheritance is an evolutionary unstable trait. Muller's ratchet is escaped by episodes of paternal leakage or biparental transmission. However, to avoid the spread of selfish cytoplasmic elements, uniparental inheritance evolves again independently.
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    Replication of mitochondrial DNA: The art of staying paired to avoid dangerous changes (comment on DOI 10.1002/bies.201400052) (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-10-11
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    BioEssays 11∕2014 (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-10-11
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    Sonic the Hedgehog: A game about aging? Emerging evidence for anti-geriatric effects of Hedgehog signaling (retrospective on DOI 10.1002/bies.201200049) (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-09-30
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    Divide and conquer: The surprising link between motility and the cell cycle (retrospective on DOI 10.1002/bies.201200119) (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-09-30
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    Microtubules as key coordinators of nuclear envelope and endoplasmic reticulum dynamics during mitosis (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-05-22
    Description: During mitosis, cells comprehensively restructure their interior to promote the faithful inheritance of DNA and cytoplasmic contents. In metazoans, this restructuring entails disassembly of the nuclear envelope, redistribution of its components into the endoplasmic reticulum (ER) and eventually nuclear envelope reassembly around the segregated chromosomes. The microtubule cytoskeleton has recently emerged as a critical regulator of mitotic nuclear envelope and ER dynamics. Microtubules and associated molecular motors tear open the nuclear envelope in prophase and remove nuclear envelope remnants from chromatin. Additionally, two distinct mechanisms of microtubule-based regulation of ER dynamics operate later in mitosis. First, association of the ER with microtubules is reduced, preventing invasion of ER into the spindle area, and second, organelle membrane is actively cleared from metaphase chromosomes. However, we are only beginning to understand the role of microtubules in shaping and distributing ER and other organelles during mitosis. Division of eukaryotic cells requires extensive remodeling of the cellular interior, including that of most membrane-bound organelles. In the course of mitosis, the endoplasmic reticulum and nuclear envelope undergo stage-specific restructuring events. Proteins mediating interactions between the endoplasmic reticulum and microtubules are key players in these events.
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    Reflecting on 30 years of BioEssays (2014)
    Wiley
    In: BioEssays
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    Publication Date: 2014-06-06
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