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  • 1
    Publication Date: 2010-10-29
    Description: Biodiversity is rapidly declining, and this may negatively affect ecosystem processes, including economically important ecosystem services. Previous studies have shown that biodiversity has positive effects on organisms and processes across trophic levels. However, only a few studies have so far incorporated an explicit food-web perspective. In an eight-year biodiversity experiment, we studied an unprecedented range of above- and below-ground organisms and multitrophic interactions. A multitrophic data set originating from a single long-term experiment allows mechanistic insights that would not be gained from meta-analysis of different experiments. Here we show that plant diversity effects dampen with increasing trophic level and degree of omnivory. This was true both for abundance and species richness of organisms. Furthermore, we present comprehensive above-ground/below-ground biodiversity food webs. Both above ground and below ground, herbivores responded more strongly to changes in plant diversity than did carnivores or omnivores. Density and richness of carnivorous taxa was independent of vegetation structure. Below-ground responses to plant diversity were consistently weaker than above-ground responses. Responses to increasing plant diversity were generally positive, but were negative for biological invasion, pathogen infestation and hyperparasitism. Our results suggest that plant diversity has strong bottom-up effects on multitrophic interaction networks, with particularly strong effects on lower trophic levels. Effects on higher trophic levels are indirectly mediated through bottom-up trophic cascades.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scherber, Christoph -- Eisenhauer, Nico -- Weisser, Wolfgang W -- Schmid, Bernhard -- Voigt, Winfried -- Fischer, Markus -- Schulze, Ernst-Detlef -- Roscher, Christiane -- Weigelt, Alexandra -- Allan, Eric -- Bessler, Holger -- Bonkowski, Michael -- Buchmann, Nina -- Buscot, Francois -- Clement, Lars W -- Ebeling, Anne -- Engels, Christof -- Halle, Stefan -- Kertscher, Ilona -- Klein, Alexandra-Maria -- Koller, Robert -- Konig, Stephan -- Kowalski, Esther -- Kummer, Volker -- Kuu, Annely -- Lange, Markus -- Lauterbach, Dirk -- Middelhoff, Cornelius -- Migunova, Varvara D -- Milcu, Alexandru -- Muller, Ramona -- Partsch, Stephan -- Petermann, Jana S -- Renker, Carsten -- Rottstock, Tanja -- Sabais, Alexander -- Scheu, Stefan -- Schumacher, Jens -- Temperton, Vicky M -- Tscharntke, Teja -- England -- Nature. 2010 Nov 25;468(7323):553-6. doi: 10.1038/nature09492. Epub 2010 Oct 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Georg-August-University Gottingen, Department of Crop Sciences, Agroecology, Grisebachstrasse 6, 37077 Gottingen, Germany. christoph.scherber@agr.uni-goettingen.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20981010" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biodiversity ; *Models, Biological ; *Plant Physiological Phenomena ; Population Density
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  • 2
    Publication Date: 2008-12-02
    Description: MicroRNAs comprise a broad class of small non-coding RNAs that control expression of complementary target messenger RNAs. Dysregulation of microRNAs by several mechanisms has been described in various disease states including cardiac disease. Whereas previous studies of cardiac disease have focused on microRNAs that are primarily expressed in cardiomyocytes, the role of microRNAs expressed in other cell types of the heart is unclear. Here we show that microRNA-21 (miR-21, also known as Mirn21) regulates the ERK-MAP kinase signalling pathway in cardiac fibroblasts, which has impacts on global cardiac structure and function. miR-21 levels are increased selectively in fibroblasts of the failing heart, augmenting ERK-MAP kinase activity through inhibition of sprouty homologue 1 (Spry1). This mechanism regulates fibroblast survival and growth factor secretion, apparently controlling the extent of interstitial fibrosis and cardiac hypertrophy. In vivo silencing of miR-21 by a specific antagomir in a mouse pressure-overload-induced disease model reduces cardiac ERK-MAP kinase activity, inhibits interstitial fibrosis and attenuates cardiac dysfunction. These findings reveal that microRNAs can contribute to myocardial disease by an effect in cardiac fibroblasts. Our results validate miR-21 as a disease target in heart failure and establish the therapeutic efficacy of microRNA therapeutic intervention in a cardiovascular disease setting.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thum, Thomas -- Gross, Carina -- Fiedler, Jan -- Fischer, Thomas -- Kissler, Stephan -- Bussen, Markus -- Galuppo, Paolo -- Just, Steffen -- Rottbauer, Wolfgang -- Frantz, Stefan -- Castoldi, Mirco -- Soutschek, Jurgen -- Koteliansky, Victor -- Rosenwald, Andreas -- Basson, M Albert -- Licht, Jonathan D -- Pena, John T R -- Rouhanifard, Sara H -- Muckenthaler, Martina U -- Tuschl, Thomas -- Martin, Gail R -- Bauersachs, Johann -- Engelhardt, Stefan -- R01 CA059998/CA/NCI NIH HHS/ -- R01 CA78711/CA/NCI NIH HHS/ -- England -- Nature. 2008 Dec 18;456(7224):980-4. doi: 10.1038/nature07511. Epub 2008 Nov 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine I, Interdisziplinares Zentrum fur Klinische Forschung (IZKF), University of Wuerzburg, 97080 Wuerzburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19043405" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cardiomyopathies/*genetics/*metabolism/pathology/therapy ; Cell Line ; Cell Survival ; Cells, Cultured ; Disease Models, Animal ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Fibroblasts/*metabolism ; Gene Silencing ; Humans ; *MAP Kinase Signaling System ; Male ; Mice ; Mice, Transgenic ; MicroRNAs/*genetics ; Myocytes, Cardiac/cytology/metabolism ; Rats
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  • 3
    Publication Date: 2008-06-06
    Description: Drosophila neuroblasts and ovarian stem cells are well characterized models for stem cell biology. In both cell types, one daughter cell self-renews continuously while the other undergoes a limited number of divisions, stops to proliferate mitotically and differentiates. Whereas neuroblasts segregate the Trim-NHL (tripartite motif and Ncl-1, HT2A and Lin-41 domain)-containing protein Brain tumour (Brat) into one of the two daughter cells, ovarian stem cells are regulated by an extracellular signal from the surrounding stem cell niche. After division, one daughter cell looses niche contact. It undergoes 4 transit-amplifying divisions to form a cyst of 16 interconnected cells that reduce their rate of growth and stop to proliferate mitotically. Here we show that the Trim-NHL protein Mei-P26 (refs 7, 8) restricts growth and proliferation in the ovarian stem cell lineage. Mei-P26 expression is low in stem cells but is strongly induced in 16-cell cysts. In mei-P26 mutants, transit-amplifying cells are larger and proliferate indefinitely leading to the formation of an ovarian tumour. Like brat, mei-P26 regulates nucleolar size and can induce differentiation in Drosophila neuroblasts, suggesting that these genes act through the same pathway. We identify Argonaute-1, a component of the RISC complex, as a common binding partner of Brat and Mei-P26, and show that Mei-P26 acts by inhibiting the microRNA pathway. Mei-P26 and Brat have a similar domain composition that is also found in other tumour suppressors and might be a defining property of a new family of microRNA regulators that act specifically in stem cell lineages.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2988194/" 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/PMC2988194/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Neumuller, Ralph A -- Betschinger, Joerg -- Fischer, Anja -- Bushati, Natascha -- Poernbacher, Ingrid -- Mechtler, Karl -- Cohen, Stephen M -- Knoblich, Juergen A -- P 16629/Austrian Science Fund FWF/Austria -- England -- Nature. 2008 Jul 10;454(7201):241-5. doi: 10.1038/nature07014. Epub 2008 Jun 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Dr Bohr Gasse 3, 1030 Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18528333" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argonaute Proteins ; Cell Cycle ; Cell Differentiation ; Cell Enlargement ; Cell Line ; *Cell Lineage ; Cell Nucleolus/metabolism ; Cell Size ; DNA-Binding Proteins/metabolism ; Drosophila Proteins/genetics/*metabolism ; Drosophila melanogaster/classification/*cytology/genetics ; Eukaryotic Initiation Factors ; Female ; MicroRNAs/genetics/*metabolism ; Mutation ; Neurons/cytology/metabolism ; Ovary/*cytology/metabolism ; Stem Cells/*cytology/*metabolism
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  • 4
    Publication Date: 2008-04-11
    Description: Terrestrial vegetation, especially tropical rain forest, releases vast quantities of volatile organic compounds (VOCs) to the atmosphere, which are removed by oxidation reactions and deposition of reaction products. The oxidation is mainly initiated by hydroxyl radicals (OH), primarily formed through the photodissociation of ozone. Previously it was thought that, in unpolluted air, biogenic VOCs deplete OH and reduce the atmospheric oxidation capacity. Conversely, in polluted air VOC oxidation leads to noxious oxidant build-up by the catalytic action of nitrogen oxides (NO(x) = NO + NO2). Here we report aircraft measurements of atmospheric trace gases performed over the pristine Amazon forest. Our data reveal unexpectedly high OH concentrations. We propose that natural VOC oxidation, notably of isoprene, recycles OH efficiently in low-NO(x) air through reactions of organic peroxy radicals. Computations with an atmospheric chemistry model and the results of laboratory experiments suggest that an OH recycling efficiency of 40-80 per cent in isoprene oxidation may be able to explain the high OH levels we observed in the field. Although further laboratory studies are necessary to explore the chemical mechanism responsible for OH recycling in more detail, our results demonstrate that the biosphere maintains a remarkable balance with the atmospheric environment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lelieveld, J -- Butler, T M -- Crowley, J N -- Dillon, T J -- Fischer, H -- Ganzeveld, L -- Harder, H -- Lawrence, M G -- Martinez, M -- Taraborrelli, D -- Williams, J -- England -- Nature. 2008 Apr 10;452(7188):737-40. doi: 10.1038/nature06870.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute for Chemistry, 27 Becherweg, 55128 Mainz, Germany. lelieveld@mpch-mainz.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18401407" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atlantic Ocean ; Atmosphere/*chemistry ; Butadienes/metabolism ; French Guiana ; Guyana ; Hemiterpenes/metabolism ; Hydroxyl Radical/metabolism ; Nitric Oxide/metabolism ; Oxidation-Reduction ; Ozone/analysis ; Pentanes/metabolism ; Suriname ; Trees/*metabolism ; *Tropical Climate
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2008-09-12
    Description: Mutations that enhance the response to double-stranded RNA (dsRNA) have revealed components of the RNA interference (RNAi) pathway or related small RNA pathways. To explore these small RNA pathways, we screened for Caenorhabditis elegans mutants displaying an enhanced response to exogenous dsRNAs. Here we describe the isolation of mutations in two adjacent, divergently transcribed open reading frames (eri-6 and eri-7) that fail to complement. eri-6 and eri-7 produce separate pre-messenger RNAs (pre-mRNAs) that are trans-spliced to form a functional mRNA, eri-6/7. Trans-splicing of eri-6/7 is mediated by a direct repeat that flanks the eri-6 gene. Adenosine to inosine editing within untranslated regions of eri-6 and eri-7 pre-mRNAs reveals a double-stranded pre-mRNA intermediate, forming in the nucleus before splicing occurs. The ERI-6/7 protein is a superfamily I helicase that both negatively regulates the exogenous RNAi pathway and functions in an endogenous RNAi pathway.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756026/" 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/PMC2756026/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fischer, Sylvia E J -- Butler, Maurice D -- Pan, Qi -- Ruvkun, Gary -- R01 GM044619/GM/NIGMS NIH HHS/ -- R01 GM044619-17/GM/NIGMS NIH HHS/ -- England -- Nature. 2008 Sep 25;455(7212):491-6. doi: 10.1038/nature07274. Epub 2008 Sep 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18784652" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/classification/*genetics/*metabolism ; Caenorhabditis elegans Proteins/*genetics/*metabolism ; DNA Helicases/*genetics/*metabolism ; Genes, Helminth/*genetics ; Genetic Complementation Test ; Molecular Sequence Data ; Mutation/genetics ; Open Reading Frames/genetics ; RNA Interference/*physiology ; Repetitive Sequences, Nucleic Acid/genetics ; *Trans-Splicing
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  • 6
    Publication Date: 2009-03-13
    Description: Behavioural responses to wind are thought to have a critical role in controlling the dispersal and population genetics of wild Drosophila species, as well as their navigation in flight, but their underlying neurobiological basis is unknown. We show that Drosophila melanogaster, like wild-caught Drosophila strains, exhibits robust wind-induced suppression of locomotion in response to air currents delivered at speeds normally encountered in nature. Here we identify wind-sensitive neurons in Johnston's organ, an antennal mechanosensory structure previously implicated in near-field sound detection (reviewed in refs 5 and 6). Using enhancer trap lines targeted to different subsets of Johnston's organ neurons, and a genetically encoded calcium indicator, we show that wind and near-field sound (courtship song) activate distinct populations of Johnston's organ neurons, which project to different regions of the antennal and mechanosensory motor centre in the central brain. Selective genetic ablation of wind-sensitive Johnston's organ neurons in the antenna abolishes wind-induced suppression of locomotion behaviour, without impairing hearing. Moreover, different neuronal subsets within the wind-sensitive population respond to different directions of arista deflection caused by air flow and project to different regions of the antennal and mechanosensory motor centre, providing a rudimentary map of wind direction in the brain. Importantly, sound- and wind-sensitive Johnston's organ neurons exhibit different intrinsic response properties: the former are phasically activated by small, bi-directional, displacements of the aristae, whereas the latter are tonically activated by unidirectional, static deflections of larger magnitude. These different intrinsic properties are well suited to the detection of oscillatory pulses of near-field sound and laminar air flow, respectively. These data identify wind-sensitive neurons in Johnston's organ, a structure that has been primarily associated with hearing, and reveal how the brain can distinguish different types of air particle movements using a common sensory organ.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2755041/" 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/PMC2755041/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yorozu, Suzuko -- Wong, Allan -- Fischer, Brian J -- Dankert, Heiko -- Kernan, Maurice J -- Kamikouchi, Azusa -- Ito, Kei -- Anderson, David J -- R01 DC002780/DC/NIDCD NIH HHS/ -- T32 GM007737/GM/NIGMS NIH HHS/ -- T32 GM007737-30/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Mar 12;458(7235):201-5. doi: 10.1038/nature07843.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology 216-76, California Institute of Technology, Pasadena, California 91125, USA. yorozu@caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19279637" target="_blank"〉PubMed〈/a〉
    Keywords: *Air Movements ; Animals ; Auditory Perception/*physiology ; Behavior, Animal/physiology ; Drosophila melanogaster/*physiology ; Electrophysiological Phenomena/physiology ; Mechanoreceptors/physiology ; Sensory Receptor Cells/*physiology
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  • 7
    Publication Date: 2009-09-26
    Description: Reconstructions of atmospheric CO(2) concentrations based on Antarctic ice cores reveal significant changes during the Holocene epoch, but the processes responsible for these changes in CO(2) concentrations have not been unambiguously identified. Distinct characteristics in the carbon isotope signatures of the major carbon reservoirs (ocean, biosphere, sediments and atmosphere) constrain variations in the CO(2) fluxes between those reservoirs. Here we present a highly resolved atmospheric delta(13)C record for the past 11,000 years from measurements on atmospheric CO(2) trapped in an Antarctic ice core. From mass-balance inverse model calculations performed with a simplified carbon cycle model, we show that the decrease in atmospheric CO(2) of about 5 parts per million by volume (p.p.m.v.). The increase in delta(13)C of about 0.25 per thousand during the early Holocene is most probably the result of a combination of carbon uptake of about 290 gigatonnes of carbon by the land biosphere and carbon release from the ocean in response to carbonate compensation of the terrestrial uptake during the termination of the last ice age. The 20 p.p.m.v. increase of atmospheric CO(2) and the small decrease in delta(13)C of about 0.05 per thousand during the later Holocene can mostly be explained by contributions from carbonate compensation of earlier land-biosphere uptake and coral reef formation, with only a minor contribution from a small decrease of the land-biosphere carbon inventory.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elsig, Joachim -- Schmitt, Jochen -- Leuenberger, Daiana -- Schneider, Robert -- Eyer, Marc -- Leuenberger, Markus -- Joos, Fortunat -- Fischer, Hubertus -- Stocker, Thomas F -- England -- Nature. 2009 Sep 24;461(7263):507-10. doi: 10.1038/nature08393.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Climate and Environmental Physics, Physics Institute, University of Bern, Sidlerstrasse 5, CH-3012 Bern, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19779448" target="_blank"〉PubMed〈/a〉
    Keywords: Air/analysis ; Animals ; Antarctic Regions ; Anthozoa/growth & development/metabolism ; Atmosphere/chemistry ; Carbon/*analysis/*metabolism ; Carbon Dioxide/analysis/*metabolism ; Carbon Isotopes ; Climate ; Ecosystem ; History, Ancient ; Ice Cover/*chemistry ; Time Factors
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  • 8
    Publication Date: 2009-02-24
    Description: Several independent, genome-wide association studies have identified a strong correlation between body mass index and polymorphisms in the human FTO gene. Common variants in the first intron define a risk allele predisposing to obesity, with homozygotes for the risk allele weighing approximately 3 kilograms more than homozygotes for the low risk allele. Nevertheless, the functional role of FTO in energy homeostasis remains elusive. Here we show that the loss of Fto in mice leads to postnatal growth retardation and a significant reduction in adipose tissue and lean body mass. The leanness of Fto-deficient mice develops as a consequence of increased energy expenditure and systemic sympathetic activation, despite decreased spontaneous locomotor activity and relative hyperphagia. Taken together, these experiments provide, to our knowledge, the first direct demonstration that Fto is functionally involved in energy homeostasis by the control of energy expenditure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fischer, Julia -- Koch, Linda -- Emmerling, Christian -- Vierkotten, Jeanette -- Peters, Thomas -- Bruning, Jens C -- Ruther, Ulrich -- England -- Nature. 2009 Apr 16;458(7240):894-8. doi: 10.1038/nature07848. Epub 2009 Feb 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Animal Developmental and Molecular Biology, Heinrich Heine University, Universitatsstr. 1, D-40225 Dusseldorf, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19234441" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/metabolism ; Adiposity/genetics ; Animals ; Animals, Newborn ; Body Weight/genetics ; Brain/metabolism ; Eating/physiology ; Embryo, Mammalian/anatomy & histology/embryology ; Energy Metabolism/genetics/physiology ; Female ; Growth Disorders/genetics/physiopathology ; Homozygote ; Hyperphagia/genetics ; Insulin/metabolism ; Male ; Mice ; Mixed Function Oxygenases ; Motor Activity/genetics/physiology ; Obesity/*genetics/prevention & control ; Oxo-Acid-Lyases/*deficiency/genetics/*metabolism ; Phenotype ; Sympathetic Nervous System/physiology ; Thinness/*genetics
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  • 9
    Publication Date: 2009-06-23
    Description: In fasted mammals, circulating pancreatic glucagon stimulates hepatic gluconeogenesis in part through the CREB regulated transcription coactivator 2 (CRTC2, also referred to as TORC2). Hepatic glucose production is increased in obesity, reflecting chronic increases in endoplasmic reticulum (ER) stress that promote insulin resistance. Whether ER stress also modulates the gluconeogenic program directly, however, is unclear. Here we show that CRTC2 functions as a dual sensor for ER stress and fasting signals. Acute increases in ER stress triggered the dephosphorylation and nuclear entry of CRTC2, which in turn promoted the expression of ER quality control genes through an association with activating transcription factor 6 alpha (ATF6alpha, also known as ATF6)--an integral branch of the unfolded protein response. In addition to mediating CRTC2 recruitment to ER stress inducible promoters, ATF6alpha also reduced hepatic glucose output by disrupting the CREB-CRTC2 interaction and thereby inhibiting CRTC2 occupancy over gluconeogenic genes. Conversely, hepatic glucose output was upregulated when hepatic ATF6alpha protein amounts were reduced, either by RNA interference (RNAi)-mediated knockdown or as a result of persistent stress in obesity. Because ATF6alpha overexpression in the livers of obese mice reversed CRTC2 effects on the gluconeogenic program and lowered hepatic glucose output, our results demonstrate how cross-talk between ER stress and fasting pathways at the level of a transcriptional coactivator contributes to glucose homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2730924/" 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/PMC2730924/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Yiguo -- Vera, Liliana -- Fischer, Wolfgang H -- Montminy, Marc -- R01 DK064142/DK/NIDDK NIH HHS/ -- R01 DK064142-06/DK/NIDDK NIH HHS/ -- R01 DK083834/DK/NIDDK NIH HHS/ -- R01 DK083834-25/DK/NIDDK NIH HHS/ -- R37 DK083834/DK/NIDDK NIH HHS/ -- England -- Nature. 2009 Jul 23;460(7254):534-7. doi: 10.1038/nature08111. Epub 2009 Jun 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Clayton Foundation Laboratories for Peptide Biology, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19543265" target="_blank"〉PubMed〈/a〉
    Keywords: Activating Transcription Factor 6 ; Animals ; Cell Nucleus/metabolism ; Cyclic AMP Response Element-Binding Protein/metabolism ; Endoplasmic Reticulum/*metabolism ; Fasting/*physiology ; Gene Expression Regulation ; Gluconeogenesis/*physiology ; Liver/*metabolism ; Male ; Membrane Proteins/metabolism ; Mice ; Obesity/physiopathology ; Protein Transport ; Stress, Physiological/*physiology ; Trans-Activators/*metabolism ; Transcription Factors/*metabolism
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  • 10
    Publication Date: 2012-06-23
    Description: Two African apes are the closest living relatives of humans: the chimpanzee (Pan troglodytes) and the bonobo (Pan paniscus). Although they are similar in many respects, bonobos and chimpanzees differ strikingly in key social and sexual behaviours, and for some of these traits they show more similarity with humans than with each other. Here we report the sequencing and assembly of the bonobo genome to study its evolutionary relationship with the chimpanzee and human genomes. We find that more than three per cent of the human genome is more closely related to either the bonobo or the chimpanzee genome than these are to each other. These regions allow various aspects of the ancestry of the two ape species to be reconstructed. In addition, many of the regions that overlap genes may eventually help us understand the genetic basis of phenotypes that humans share with one of the two apes to the exclusion of the other.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3498939/" 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/PMC3498939/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Prufer, Kay -- Munch, Kasper -- Hellmann, Ines -- Akagi, Keiko -- Miller, Jason R -- Walenz, Brian -- Koren, Sergey -- Sutton, Granger -- Kodira, Chinnappa -- Winer, Roger -- Knight, James R -- Mullikin, James C -- Meader, Stephen J -- Ponting, Chris P -- Lunter, Gerton -- Higashino, Saneyuki -- Hobolth, Asger -- Dutheil, Julien -- Karakoc, Emre -- Alkan, Can -- Sajjadian, Saba -- Catacchio, Claudia Rita -- Ventura, Mario -- Marques-Bonet, Tomas -- Eichler, Evan E -- Andre, Claudine -- Atencia, Rebeca -- Mugisha, Lawrence -- Junhold, Jorg -- Patterson, Nick -- Siebauer, Michael -- Good, Jeffrey M -- Fischer, Anne -- Ptak, Susan E -- Lachmann, Michael -- Symer, David E -- Mailund, Thomas -- Schierup, Mikkel H -- Andres, Aida M -- Kelso, Janet -- Paabo, Svante -- 090532/Wellcome Trust/United Kingdom -- 090532/Z/09/Z/Wellcome Trust/United Kingdom -- 2R01GM077117-04A1/GM/NIGMS NIH HHS/ -- HG002385/HG/NHGRI NIH HHS/ -- MC_U137761446/Medical Research Council/United Kingdom -- R01 GM077117/GM/NIGMS NIH HHS/ -- R01 HG002385/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- England -- Nature. 2012 Jun 28;486(7404):527-31. doi: 10.1038/nature11128.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute for Evolutionary Anthropology, D-04103 Leipzig, Germany. pruefer@eva.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22722832" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA Transposable Elements/genetics ; *Evolution, Molecular ; Gene Duplication/genetics ; Genetic Variation/*genetics ; Genome/*genetics ; Genome, Human/*genetics ; Genotype ; Humans ; Molecular Sequence Data ; Pan paniscus/*genetics ; Pan troglodytes/*genetics ; Phenotype ; Phylogeny ; Species Specificity
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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