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  • Animals  (27)
  • Electronic structure and strongly correlated systems
  • Nature Publishing Group (NPG)  (27)
  • 1
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    Negative plant-soil feedback predicts tree-species relative abundance in a tropical forest (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-06-29
    Description: The accumulation of species-specific enemies around adults is hypothesized to maintain plant diversity by limiting the recruitment of conspecific seedlings relative to heterospecific seedlings. Although previous studies in forested ecosystems have documented patterns consistent with the process of negative feedback, these studies are unable to address which classes of enemies (for example, pathogens, invertebrates, mammals) exhibit species-specific effects strong enough to generate negative feedback, and whether negative feedback at the level of the individual tree is sufficient to influence community-wide forest composition. Here we use fully reciprocal shade-house and field experiments to test whether the performance of conspecific tree seedlings (relative to heterospecific seedlings) is reduced when grown in the presence of enemies associated with adult trees. Both experiments provide strong evidence for negative plant-soil feedback mediated by soil biota. In contrast, above-ground enemies (mammals, foliar herbivores and foliar pathogens) contributed little to negative feedback observed in the field. In both experiments, we found that tree species that showed stronger negative feedback were less common as adults in the forest community, indicating that susceptibility to soil biota may determine species relative abundance in these tropical forests. Finally, our simulation models confirm that the strength of local negative feedback that we measured is sufficient to produce the observed community-wide patterns in tree-species relative abundance. Our findings indicate that plant-soil feedback is an important mechanism that can maintain species diversity and explain patterns of tree-species relative abundance in tropical forests.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mangan, Scott A -- Schnitzer, Stefan A -- Herre, Edward A -- Mack, Keenan M L -- Valencia, Mariana C -- Sanchez, Evelyn I -- Bever, James D -- R01 GM092660/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 Aug 5;466(7307):752-5. doi: 10.1038/nature09273.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, University of Wisconsin-Milwaukee, Wisconsin 53201, USA. smangan37@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20581819" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biodiversity ; Biomass ; Computer Simulation ; Feedback, Physiological ; Food Chain ; Insects/physiology ; Models, Biological ; Panama ; Population Density ; Seedlings/growth & development ; Soil/*analysis ; *Soil Microbiology ; Species Specificity ; Trees/*classification/*growth & development/microbiology/parasitology ; *Tropical Climate ; Vertebrates/physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    Developmental biology: A cellular view of regeneration (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-07-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanchez Alvarado, Alejandro -- England -- Nature. 2009 Jul 2;460(7251):39-40. doi: 10.1038/460039a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19571870" target="_blank"〉PubMed〈/a〉
    Keywords: Ambystoma/embryology/*physiology ; Animals ; Cell Differentiation/radiation effects ; Cell Lineage/*physiology/radiation effects ; Extremities/*growth & development/innervation ; Organ Specificity ; Regeneration/*physiology
    Print ISSN: 0028-0836
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  • 3
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    The insect nephrocyte is a podocyte-like cell with a filtration slit diaphragm (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-10-31
    Description: The nephron is the basic structural and functional unit of the vertebrate kidney. It is composed of a glomerulus, the site of ultrafiltration, and a renal tubule, along which the filtrate is modified. Although widely regarded as a vertebrate adaptation, 'nephron-like' features can be found in the excretory systems of many invertebrates, raising the possibility that components of the vertebrate excretory system were inherited from their invertebrate ancestors. Here we show that the insect nephrocyte has remarkable anatomical, molecular and functional similarity to the glomerular podocyte, a cell in the vertebrate kidney that forms the main size-selective barrier as blood is ultrafiltered to make urine. In particular, both cell types possess a specialized filtration diaphragm, known as the slit diaphragm in podocytes or the nephrocyte diaphragm in nephrocytes. We find that fly (Drosophila melanogaster) orthologues of the major constituents of the slit diaphragm, including nephrin, NEPH1 (also known as KIRREL), CD2AP, ZO-1 (TJP1) and podocin, are expressed in the nephrocyte and form a complex of interacting proteins that closely mirrors the vertebrate slit diaphragm complex. Furthermore, we find that the nephrocyte diaphragm is completely lost in flies lacking the orthologues of nephrin or NEPH1-a phenotype resembling loss of the slit diaphragm in the absence of either nephrin (as in human congenital nephrotic syndrome of the Finnish type, NPHS1) or NEPH1. These changes markedly impair filtration function in the nephrocyte. The similarities we describe between invertebrate nephrocytes and vertebrate podocytes provide evidence suggesting that the two cell types are evolutionarily related, and establish the nephrocyte as a simple model in which to study podocyte biology and podocyte-associated diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2687078/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2687078/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weavers, Helen -- Prieto-Sanchez, Silvia -- Grawe, Ferdinand -- Garcia-Lopez, Amparo -- Artero, Ruben -- Wilsch-Brauninger, Michaela -- Ruiz-Gomez, Mar -- Skaer, Helen -- Denholm, Barry -- 072441/Wellcome Trust/United Kingdom -- 079221/Wellcome Trust/United Kingdom -- Arthritis Research UK/United Kingdom -- England -- Nature. 2009 Jan 15;457(7227):322-6. doi: 10.1038/nature07526. Epub 2008 Oct 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, University of Cambridge, Downing Street, Cambridge CB2 3EJ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18971929" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Drosophila Proteins/genetics/*metabolism ; Drosophila melanogaster/anatomy & histology/*cytology/physiology ; Immunoglobulins/genetics/metabolism ; Membrane Proteins/deficiency/genetics/metabolism ; Muscle Proteins/genetics/metabolism ; Podocytes/*cytology/metabolism/*physiology
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  • 4
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    A methyl transferase links the circadian clock to the regulation of alternative splicing (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-10-22
    Description: Circadian rhythms allow organisms to time biological processes to the most appropriate phases of the day-night cycle. Post-transcriptional regulation is emerging as an important component of circadian networks, but the molecular mechanisms linking the circadian clock to the control of RNA processing are largely unknown. Here we show that PROTEIN ARGININE METHYL TRANSFERASE 5 (PRMT5), which transfers methyl groups to arginine residues present in histones and Sm spliceosomal proteins, links the circadian clock to the control of alternative splicing in plants. Mutations in PRMT5 impair several circadian rhythms in Arabidopsis thaliana and this phenotype is caused, at least in part, by a strong alteration in alternative splicing of the core-clock gene PSEUDO RESPONSE REGULATOR 9 (PRR9). Furthermore, genome-wide studies show that PRMT5 contributes to the regulation of many pre-messenger-RNA splicing events, probably by modulating 5'-splice-site recognition. PRMT5 expression shows daily and circadian oscillations, and this contributes to the mediation of the circadian regulation of expression and alternative splicing of a subset of genes. Circadian rhythms in locomotor activity are also disrupted in dart5-1, a mutant affected in the Drosophila melanogaster PRMT5 homologue, and this is associated with alterations in splicing of the core-clock gene period and several clock-associated genes. Our results demonstrate a key role for PRMT5 in the regulation of alternative splicing and indicate that the interplay between the circadian clock and the regulation of alternative splicing by PRMT5 constitutes a common mechanism that helps organisms to synchronize physiological processes with daily changes in environmental conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanchez, Sabrina E -- Petrillo, Ezequiel -- Beckwith, Esteban J -- Zhang, Xu -- Rugnone, Matias L -- Hernando, C Esteban -- Cuevas, Juan C -- Godoy Herz, Micaela A -- Depetris-Chauvin, Ana -- Simpson, Craig G -- Brown, John W S -- Cerdan, Pablo D -- Borevitz, Justin O -- Mas, Paloma -- Ceriani, M Fernanda -- Kornblihtt, Alberto R -- Yanovsky, Marcelo J -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Nov 4;468(7320):112-6. doi: 10.1038/nature09470. Epub 2010 Oct 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉IFEVA, Facultad de Agronomia, UBA-CONICET, C1417DSE Buenos Aires, Argentina.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20962777" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing/*genetics ; Animals ; Arabidopsis/enzymology/genetics/*physiology/radiation effects ; Arabidopsis Proteins/genetics/*metabolism ; Base Sequence ; Circadian Clocks/genetics/*physiology ; Circadian Rhythm/genetics/*physiology ; Darkness ; Drosophila Proteins/genetics/*metabolism ; Drosophila melanogaster/enzymology/genetics/*physiology/radiation effects ; Gene Expression Profiling ; Gene Expression Regulation, Plant ; Light ; Methylation ; Mutation ; Period Circadian Proteins/genetics ; Phenotype ; Protein Methyltransferases/genetics/*metabolism ; Protein-Arginine N-Methyltransferases/genetics/*metabolism ; RNA Precursors/genetics/metabolism ; RNA Splice Sites/genetics ; RNA, Messenger/genetics/metabolism ; Spliceosomes/metabolism ; Transcription Factors/genetics
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  • 5
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    Loss of fish actinotrichia proteins and the fin-to-limb transition (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-06-25
    Description: The early development of teleost paired fins is strikingly similar to that of tetrapod limb buds and is controlled by similar mechanisms. One early morphological divergence between pectoral fins and limbs is in the fate of the apical ectodermal ridge (AER), the distal epidermis that rims the bud. Whereas the AER of tetrapods regresses after specification of the skeletal progenitors, the AER of teleost fishes forms a fold that elongates. Formation of the fin fold is accompanied by the synthesis of two rows of rigid, unmineralized fibrils called actinotrichia, which keep the fold straight and guide the migration of mesenchymal cells within the fold. The actinotrichia are made of elastoidin, the components of which, apart from collagen, are unknown. Here we show that two zebrafish proteins, which we name actinodin 1 and 2 (And1 and And2), are essential structural components of elastoidin. The presence of actinodin sequences in several teleost fishes and in the elephant shark (Callorhinchus milii, which occupies a basal phylogenetic position), but not in tetrapods, suggests that these genes have been lost during tetrapod species evolution. Double gene knockdown of and1 and and2 in zebrafish embryos results in the absence of actinotrichia and impaired fin folds. Gene expression profiles in embryos lacking and1 and and2 function are consistent with pectoral fin truncation and may offer a potential explanation for the polydactyly observed in early tetrapod fossils. We propose that the loss of both actinodins and actinotrichia during evolution may have led to the loss of lepidotrichia and may have contributed to the fin-to-limb transition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Jing -- Wagh, Purva -- Guay, Danielle -- Sanchez-Pulido, Luis -- Padhi, Bhaja K -- Korzh, Vladimir -- Andrade-Navarro, Miguel A -- Akimenko, Marie-Andree -- MC_U137761446/Medical Research Council/United Kingdom -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2010 Jul 8;466(7303):234-7. doi: 10.1038/nature09137. Epub 2010 Jun 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CAREG, Department of Biology, University of Ottawa, Ottawa, Ontario K1N 6N5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20574421" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Structures/*anatomy & histology/embryology/*physiology ; Animals ; *Biological Evolution ; Collagen/chemistry/metabolism ; Ectoderm/embryology/metabolism ; Embryo, Nonmammalian/anatomy & histology/embryology/metabolism ; Evolution, Molecular ; Extremities/anatomy & histology/embryology/*physiology ; Fish Proteins/*deficiency/genetics/metabolism ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Gene Knockdown Techniques ; Limb Buds/anatomy & histology/embryology/metabolism ; Models, Biological ; Phylogeny ; Zebrafish/*anatomy & histology/embryology/genetics/*metabolism ; Zebrafish Proteins/deficiency/genetics/metabolism
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  • 6
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    Stage-specific sensitivity to p53 restoration during lung cancer progression (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-11-26
    Description: Tumorigenesis is a multistep process that results from the sequential accumulation of mutations in key oncogene and tumour suppressor pathways. Personalized cancer therapy that is based on targeting these underlying genetic abnormalities presupposes that sustained inactivation of tumour suppressors and activation of oncogenes is essential in advanced cancers. Mutations in the p53 tumour-suppressor pathway are common in human cancer and significant efforts towards pharmaceutical reactivation of defective p53 pathways are underway. Here we show that restoration of p53 in established murine lung tumours leads to significant but incomplete tumour cell loss specifically in malignant adenocarcinomas, but not in adenomas. We define amplification of MAPK signalling as a critical determinant of malignant progression and also a stimulator of Arf tumour-suppressor expression. The response to p53 restoration in this context is critically dependent on the expression of Arf. We propose that p53 not only limits malignant progression by suppressing the acquisition of alterations that lead to tumour progression, but also, in the context of p53 restoration, responds to increased oncogenic signalling to mediate tumour regression. Our observations also underscore that the p53 pathway is not engaged by low levels of oncogene activity that are sufficient for early stages of lung tumour development. These data suggest that restoration of pathways important in tumour progression, as opposed to initiation, may lead to incomplete tumour regression due to the stage-heterogeneity of tumour cell populations.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3003305/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3003305/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feldser, David M -- Kostova, Kamena K -- Winslow, Monte M -- Taylor, Sarah E -- Cashman, Chris -- Whittaker, Charles A -- Sanchez-Rivera, Francisco J -- Resnick, Rebecca -- Bronson, Roderick -- Hemann, Michael T -- Jacks, Tyler -- P30 CA014051/CA/NCI NIH HHS/ -- P30 CA014051-37/CA/NCI NIH HHS/ -- P30 CA014051-38/CA/NCI NIH HHS/ -- P30 CA014051-39/CA/NCI NIH HHS/ -- P30 CA014051-40/CA/NCI NIH HHS/ -- P30-CA14051/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Nov 25;468(7323):572-5. doi: 10.1038/nature09535.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Koch Institute for Integrative Cancer Research, Department of Biology, and Howard Hughes Medical Institute, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21107428" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/metabolism/*physiopathology ; Adenoma/metabolism/*physiopathology ; Animals ; Cell Proliferation ; *Disease Progression ; Lung Neoplasms/*physiopathology ; Mice ; Mice, Inbred C57BL ; Mitogen-Activated Protein Kinases/metabolism ; Signal Transduction ; Tumor Suppressor Protein p53/genetics/*metabolism
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  • 7
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    Oxidant stress evoked by pacemaking in dopaminergic neurons is attenuated by DJ-1 (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-11-12
    Description: Parkinson's disease is a pervasive, ageing-related neurodegenerative disease the cardinal motor symptoms of which reflect the loss of a small group of neurons, the dopaminergic neurons in the substantia nigra pars compacta (SNc). Mitochondrial oxidant stress is widely viewed as being responsible for this loss, but why these particular neurons should be stressed is a mystery. Here we show, using transgenic mice that expressed a redox-sensitive variant of green fluorescent protein targeted to the mitochondrial matrix, that the engagement of plasma membrane L-type calcium channels during normal autonomous pacemaking created an oxidant stress that was specific to vulnerable SNc dopaminergic neurons. The oxidant stress engaged defences that induced transient, mild mitochondrial depolarization or uncoupling. The mild uncoupling was not affected by deletion of cyclophilin D, which is a component of the permeability transition pore, but was attenuated by genipin and purine nucleotides, which are antagonists of cloned uncoupling proteins. Knocking out DJ-1 (also known as PARK7 in humans and Park7 in mice), which is a gene associated with an early-onset form of Parkinson's disease, downregulated the expression of two uncoupling proteins (UCP4 (SLC25A27) and UCP5 (SLC25A14)), compromised calcium-induced uncoupling and increased oxidation of matrix proteins specifically in SNc dopaminergic neurons. Because drugs approved for human use can antagonize calcium entry through L-type channels, these results point to a novel neuroprotective strategy for both idiopathic and familial forms of Parkinson's disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4465557/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4465557/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guzman, Jaime N -- Sanchez-Padilla, Javier -- Wokosin, David -- Kondapalli, Jyothisri -- Ilijic, Ema -- Schumacker, Paul T -- Surmeier, D James -- HL35440/HL/NHLBI NIH HHS/ -- K12GM088020/GM/NIGMS NIH HHS/ -- NS 054850/NS/NINDS NIH HHS/ -- NS047085/NS/NINDS NIH HHS/ -- P30 NS054850/NS/NINDS NIH HHS/ -- P50 NS047085/NS/NINDS NIH HHS/ -- R01 HL035440/HL/NHLBI NIH HHS/ -- R21 RR025355/RR/NCRR NIH HHS/ -- RR025355/RR/NCRR NIH HHS/ -- England -- Nature. 2010 Dec 2;468(7324):696-700. doi: 10.1038/nature09536. Epub 2010 Nov 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21068725" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks/*physiology ; Brain/cytology/metabolism ; Calcium/metabolism ; Calcium Channel Blockers/pharmacology ; Calcium Channels, L-Type/metabolism/pharmacology ; Calcium Signaling ; Cyclophilins/metabolism ; Dihydropyridines/pharmacology ; Dopamine/*metabolism ; Gene Deletion ; Ion Channels/antagonists & inhibitors/metabolism ; Iridoid Glycosides/pharmacology ; Iridoids ; Male ; Mice ; Mice, Transgenic ; Mitochondria/metabolism ; Mitochondrial Proteins/antagonists & inhibitors/metabolism ; Neurons/cytology/*metabolism ; Oncogene Proteins/deficiency/genetics/*metabolism ; *Oxidative Stress ; Parkinson Disease/metabolism/pathology/prevention & control ; Peroxiredoxins ; Purines/pharmacology ; Superoxides/metabolism
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  • 8
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    The genomes of four tapeworm species reveal adaptations to parasitism (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-03-15
    Description: Tapeworms (Cestoda) cause neglected diseases that can be fatal and are difficult to treat, owing to inefficient drugs. Here we present an analysis of tapeworm genome sequences using the human-infective species Echinococcus multilocularis, E. granulosus, Taenia solium and the laboratory model Hymenolepis microstoma as examples. The 115- to 141-megabase genomes offer insights into the evolution of parasitism. Synteny is maintained with distantly related blood flukes but we find extreme losses of genes and pathways that are ubiquitous in other animals, including 34 homeobox families and several determinants of stem cell fate. Tapeworms have specialized detoxification pathways, metabolism that is finely tuned to rely on nutrients scavenged from their hosts, and species-specific expansions of non-canonical heat shock proteins and families of known antigens. We identify new potential drug targets, including some on which existing pharmaceuticals may act. The genomes provide a rich resource to underpin the development of urgently needed treatments and control.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3964345/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3964345/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsai, Isheng J -- Zarowiecki, Magdalena -- Holroyd, Nancy -- Garciarrubio, Alejandro -- Sanchez-Flores, Alejandro -- Brooks, Karen L -- Tracey, Alan -- Bobes, Raul J -- Fragoso, Gladis -- Sciutto, Edda -- Aslett, Martin -- Beasley, Helen -- Bennett, Hayley M -- Cai, Jianping -- Camicia, Federico -- Clark, Richard -- Cucher, Marcela -- De Silva, Nishadi -- Day, Tim A -- Deplazes, Peter -- Estrada, Karel -- Fernandez, Cecilia -- Holland, Peter W H -- Hou, Junling -- Hu, Songnian -- Huckvale, Thomas -- Hung, Stacy S -- Kamenetzky, Laura -- Keane, Jacqueline A -- Kiss, Ferenc -- Koziol, Uriel -- Lambert, Olivia -- Liu, Kan -- Luo, Xuenong -- Luo, Yingfeng -- Macchiaroli, Natalia -- Nichol, Sarah -- Paps, Jordi -- Parkinson, John -- Pouchkina-Stantcheva, Natasha -- Riddiford, Nick -- Rosenzvit, Mara -- Salinas, Gustavo -- Wasmuth, James D -- Zamanian, Mostafa -- Zheng, Yadong -- Taenia solium Genome Consortium -- Cai, Xuepeng -- Soberon, Xavier -- Olson, Peter D -- Laclette, Juan P -- Brehm, Klaus -- Berriman, Matthew -- 085775/Wellcome Trust/United Kingdom -- 098051/Wellcome Trust/United Kingdom -- BBG0038151/Biotechnology and Biological Sciences Research Council/United Kingdom -- MOP#84556/Canadian Institutes of Health Research/Canada -- TW008588/TW/FIC NIH HHS/ -- England -- Nature. 2013 Apr 4;496(7443):57-63. doi: 10.1038/nature12031. Epub 2013 Mar 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Parasite Genomics, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23485966" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological/*genetics ; Animals ; Biological Evolution ; Cestoda/drug effects/*genetics/physiology ; Cestode Infections/drug therapy/metabolism ; Conserved Sequence/genetics ; Echinococcus granulosus/genetics ; Echinococcus multilocularis/drug effects/genetics/metabolism ; Genes, Helminth/genetics ; Genes, Homeobox/genetics ; Genome, Helminth/*genetics ; HSP70 Heat-Shock Proteins/genetics ; Humans ; Hymenolepis/genetics ; Metabolic Networks and Pathways/genetics ; Molecular Targeted Therapy ; Parasites/drug effects/*genetics/physiology ; Proteome/genetics ; Stem Cells/cytology/metabolism ; Taenia solium/genetics
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  • 9
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    Ultraviolet radiation accelerates BRAF-driven melanomagenesis by targeting TP53 (2014)
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    Publication Date: 2014-06-12
    Description: Cutaneous melanoma is epidemiologically linked to ultraviolet radiation (UVR), but the molecular mechanisms by which UVR drives melanomagenesis remain unclear. The most common somatic mutation in melanoma is a V600E substitution in BRAF, which is an early event. To investigate how UVR accelerates oncogenic BRAF-driven melanomagenesis, we used a BRAF(V600E) mouse model. In mice expressing BRAF(V600E) in their melanocytes, a single dose of UVR that mimicked mild sunburn in humans induced clonal expansion of the melanocytes, and repeated doses of UVR increased melanoma burden. Here we show that sunscreen (UVA superior, UVB sun protection factor (SPF) 50) delayed the onset of UVR-driven melanoma, but only provided partial protection. The UVR-exposed tumours showed increased numbers of single nucleotide variants and we observed mutations (H39Y, S124F, R245C, R270C, C272G) in the Trp53 tumour suppressor in approximately 40% of cases. TP53 is an accepted UVR target in human non-melanoma skin cancer, but is not thought to have a major role in melanoma. However, we show that, in mice, mutant Trp53 accelerated BRAF(V600E)-driven melanomagenesis, and that TP53 mutations are linked to evidence of UVR-induced DNA damage in human melanoma. Thus, we provide mechanistic insight into epidemiological data linking UVR to acquired naevi in humans. Furthermore, we identify TP53/Trp53 as a UVR-target gene that cooperates with BRAF(V600E) to induce melanoma, providing molecular insight into how UVR accelerates melanomagenesis. Our study validates public health campaigns that promote sunscreen protection for individuals at risk of melanoma.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4112218/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4112218/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Viros, Amaya -- Sanchez-Laorden, Berta -- Pedersen, Malin -- Furney, Simon J -- Rae, Joel -- Hogan, Kate -- Ejiama, Sarah -- Girotti, Maria Romina -- Cook, Martin -- Dhomen, Nathalie -- Marais, Richard -- A12738/Cancer Research UK/United Kingdom -- A13540/Cancer Research UK/United Kingdom -- A17240/Cancer Research UK/United Kingdom -- A7091/Cancer Research UK/United Kingdom -- A7192/Cancer Research UK/United Kingdom -- C107/A10433/Cancer Research UK/United Kingdom -- C5759/A12328/Cancer Research UK/United Kingdom -- England -- Nature. 2014 Jul 24;511(7510):478-82. doi: 10.1038/nature13298. Epub 2014 Jun 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Molecular Oncology Group, Cancer Research UK Manchester Institute, University of Manchester, Wilmslow Road, Manchester M20 4BX, UK [2]. ; 1] Signal Transduction Team, Institute of Cancer Research, 237 Fulham Road, London SW3 6JB, UK [2]. ; Signal Transduction Team, Institute of Cancer Research, 237 Fulham Road, London SW3 6JB, UK. ; Molecular Oncology Group, Cancer Research UK Manchester Institute, University of Manchester, Wilmslow Road, Manchester M20 4BX, UK. ; 1] Molecular Oncology Group, Cancer Research UK Manchester Institute, University of Manchester, Wilmslow Road, Manchester M20 4BX, UK [2] Histopathology, Royal Surrey County Hospital, Egerton Road, Guildford GU2 7XX, UK. ; 1] Molecular Oncology Group, Cancer Research UK Manchester Institute, University of Manchester, Wilmslow Road, Manchester M20 4BX, UK [2] Signal Transduction Team, Institute of Cancer Research, 237 Fulham Road, London SW3 6JB, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24919155" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Transformation, Neoplastic/*genetics/*radiation effects ; DNA Damage/genetics ; Disease Models, Animal ; Female ; Humans ; Melanocytes/metabolism/pathology/radiation effects ; Melanoma/etiology/*genetics/metabolism/*pathology ; Mice ; Mice, Inbred C57BL ; Mutagenesis/genetics/*radiation effects ; Mutation/genetics/radiation effects ; Nevus/etiology/genetics/metabolism/pathology ; Proto-Oncogene Proteins B-raf/*genetics/metabolism ; Skin Neoplasms/etiology/genetics/metabolism/pathology ; Sunburn/complications/etiology/genetics ; Sunscreening Agents/pharmacology ; Tumor Suppressor Protein p53/*genetics/metabolism ; Ultraviolet Rays/*adverse effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 10
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    A primitive placoderm sheds light on the origin of the jawed vertebrate face (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-02-14
    Description: Extant vertebrates form two clades, the jawless Cyclostomata (lampreys and hagfishes) and the jawed Gnathostomata (all other vertebrates), with contrasting facial architectures. These arise during development from just a few key differences in the growth patterns of the cranial primordia: notably, the nasal sacs and hypophysis originate from a single placode in cyclostomes but from separate placodes in gnathostomes, and infraoptic ectomesenchyme migrates forward either side of the single placode in cyclostomes but between the placodes in gnathostomes. Fossil stem gnathostomes preserve cranial anatomies rich in landmarks that provide proxies for developmental processes and allow the transition from jawless to jawed vertebrates to be broken down into evolutionary steps. Here we use propagation phase contrast synchrotron microtomography to image the cranial anatomy of the primitive placoderm (jawed stem gnathostome) Romundina, and show that it combines jawed vertebrate architecture with cranial and cerebral proportions resembling those of cyclostomes and the galeaspid (jawless stem gnathostome) Shuyu. This combination seems to be primitive for jawed vertebrates, and suggests a decoupling between ectomesenchymal growth trajectory, ectomesenchymal proliferation, and cerebral shape change during the origin of gnathostomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dupret, Vincent -- Sanchez, Sophie -- Goujet, Daniel -- Tafforeau, Paul -- Ahlberg, Per E -- England -- Nature. 2014 Mar 27;507(7493):500-3. doi: 10.1038/nature12980. Epub 2014 Feb 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Uppsala University, Department of Organismal Biology, Subdepartment of Evolution and Development, Norbyvagen 18A, SE-752 36, Uppsala, Sweden. ; 1] Uppsala University, Department of Organismal Biology, Subdepartment of Evolution and Development, Norbyvagen 18A, SE-752 36, Uppsala, Sweden [2] European Synchrotron Radiation Facility, 6 rue Jules Horowitz, 38043 Grenoble Cedex, France. ; Museum national d'Histoire naturelle, UMR 7207 CR2P CNRS/MNHN/UPMC, 8 rue Buffon, CP 38,75231 Paris Cedex 05, France. ; European Synchrotron Radiation Facility, 6 rue Jules Horowitz, 38043 Grenoble Cedex, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24522530" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Brain/anatomy & histology ; Face/anatomy & histology ; Fishes/*anatomy & histology/classification ; *Fossils ; *Jaw/anatomy & histology ; Lampreys/anatomy & histology ; Neural Crest/anatomy & histology ; Phylogeny
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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