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  • Female  (7)
  • Nature Publishing Group (NPG)  (7)
  • 2010-2014  (7)
  • 1
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    Human oocytes reprogram somatic cells to a pluripotent state (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-10-08
    Description: The exchange of the oocyte's genome with the genome of a somatic cell, followed by the derivation of pluripotent stem cells, could enable the generation of specific cells affected in degenerative human diseases. Such cells, carrying the patient's genome, might be useful for cell replacement. Here we report that the development of human oocytes after genome exchange arrests at late cleavage stages in association with transcriptional abnormalities. In contrast, if the oocyte genome is not removed and the somatic cell genome is merely added, the resultant triploid cells develop to the blastocyst stage. Stem cell lines derived from these blastocysts differentiate into cell types of all three germ layers, and a pluripotent gene expression program is established on the genome derived from the somatic cell. This result demonstrates the feasibility of reprogramming human cells using oocytes and identifies removal of the oocyte genome as the primary cause of developmental failure after genome exchange.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Noggle, Scott -- Fung, Ho-Lim -- Gore, Athurva -- Martinez, Hector -- Satriani, Kathleen Crumm -- Prosser, Robert -- Oum, Kiboong -- Paull, Daniel -- Druckenmiller, Sarah -- Freeby, Matthew -- Greenberg, Ellen -- Zhang, Kun -- Goland, Robin -- Sauer, Mark V -- Leibel, Rudolph L -- Egli, Dieter -- England -- Nature. 2011 Oct 5;478(7367):70-5. doi: 10.1038/nature10397.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The New York Stem Cell Foundation Laboratory, New York, New York, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21979046" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Blastocyst/cytology/metabolism ; Cell Differentiation ; *Cellular Reprogramming ; DNA Methylation ; Epigenesis, Genetic ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Genome, Human/genetics ; Germ Layers/cytology/embryology/metabolism ; Humans ; Induced Pluripotent Stem Cells/*cytology/*metabolism ; Oocyte Donation ; Oocytes/*cytology/growth & development/*physiology ; Primary Cell Culture ; Transcription, Genetic ; Triploidy ; Young Adult
    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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    Interactions between cancer stem cells and their niche govern metastatic colonization (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-12-14
    Description: Metastatic growth in distant organs is the major cause of cancer mortality. The development of metastasis is a multistage process with several rate-limiting steps. Although dissemination of tumour cells seems to be an early and frequent event, the successful initiation of metastatic growth, a process termed 'metastatic colonization', is inefficient for many cancer types and is accomplished only by a minority of cancer cells that reach distant sites. Prevalent target sites are characteristic of many tumour entities, suggesting that inadequate support by distant tissues contributes to the inefficiency of the metastatic process. Here we show that a small population of cancer stem cells is critical for metastatic colonization, that is, the initial expansion of cancer cells at the secondary site, and that stromal niche signals are crucial to this expansion process. We find that periostin (POSTN), a component of the extracellular matrix, is expressed by fibroblasts in the normal tissue and in the stroma of the primary tumour. Infiltrating tumour cells need to induce stromal POSTN expression in the secondary target organ (in this case lung) to initiate colonization. POSTN is required to allow cancer stem cell maintenance, and blocking its function prevents metastasis. POSTN recruits Wnt ligands and thereby increases Wnt signalling in cancer stem cells. We suggest that the education of stromal cells by infiltrating tumour cells is an important step in metastatic colonization and that preventing de novo niche formation may be a novel strategy for the treatment of metastatic disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malanchi, Ilaria -- Santamaria-Martinez, Albert -- Susanto, Evelyn -- Peng, Hong -- Lehr, Hans-Anton -- Delaloye, Jean-Francois -- Huelsken, Joerg -- England -- Nature. 2011 Dec 7;481(7379):85-9. doi: 10.1038/nature10694.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ecole Polytechnique Federale de Lausanne, Swiss Institute for Experimental Cancer Research and National Center of Competence in Research Molecular Oncology, 1015 Lausanne, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22158103" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/pathology ; Cell Adhesion Molecules/genetics/metabolism ; Female ; Lung Neoplasms/secondary ; Mice ; Mice, Inbred C57BL ; Neoplasm Metastasis/*pathology ; Neoplastic Stem Cells/metabolism/*pathology ; Stem Cell Niche/*physiology ; Stromal Cells/metabolism ; Wnt Signaling Pathway
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    CLP1 links tRNA metabolism to progressive motor-neuron loss (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-03-12
    Description: CLP1 was the first mammalian RNA kinase to be identified. However, determining its in vivo function has been elusive. Here we generated kinase-dead Clp1 (Clp1(K/K)) mice that show a progressive loss of spinal motor neurons associated with axonal degeneration in the peripheral nerves and denervation of neuromuscular junctions, resulting in impaired motor function, muscle weakness, paralysis and fatal respiratory failure. Transgenic rescue experiments show that CLP1 functions in motor neurons. Mechanistically, loss of CLP1 activity results in accumulation of a novel set of small RNA fragments, derived from aberrant processing of tyrosine pre-transfer RNA. These tRNA fragments sensitize cells to oxidative-stress-induced p53 (also known as TRP53) activation and p53-dependent cell death. Genetic inactivation of p53 rescues Clp1(K/K) mice from the motor neuron loss, muscle denervation and respiratory failure. Our experiments uncover a mechanistic link between tRNA processing, formation of a new RNA species and progressive loss of lower motor neurons regulated by p53.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3674495/" 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/PMC3674495/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanada, Toshikatsu -- Weitzer, Stefan -- Mair, Barbara -- Bernreuther, Christian -- Wainger, Brian J -- Ichida, Justin -- Hanada, Reiko -- Orthofer, Michael -- Cronin, Shane J -- Komnenovic, Vukoslav -- Minis, Adi -- Sato, Fuminori -- Mimata, Hiromitsu -- Yoshimura, Akihiko -- Tamir, Ido -- Rainer, Johannes -- Kofler, Reinhard -- Yaron, Avraham -- Eggan, Kevin C -- Woolf, Clifford J -- Glatzel, Markus -- Herbst, Ruth -- Martinez, Javier -- Penninger, Josef M -- K99NS077435-01A1/NS/NINDS NIH HHS/ -- NS038253/NS/NINDS NIH HHS/ -- P 19223/Austrian Science Fund FWF/Austria -- P 21667/Austrian Science Fund FWF/Austria -- R00 NS077435/NS/NINDS NIH HHS/ -- R01 NS038253/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Mar 28;495(7442):474-80. doi: 10.1038/nature11923. Epub 2013 Mar 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉IMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Vienna 1030, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23474986" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis ; Animals ; Animals, Newborn ; Axons/metabolism/pathology ; Cell Death ; Diaphragm/innervation ; Embryo Loss ; Embryo, Mammalian/metabolism/pathology ; Exons/genetics ; Female ; Fibroblasts ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Motor Neurons/*metabolism/*pathology ; Muscular Atrophy, Spinal ; Neuromuscular Diseases/metabolism/pathology ; Oxidative Stress ; RNA Processing, Post-Transcriptional ; RNA, Transfer, Tyr/genetics/*metabolism ; Respiration ; Spinal Nerves/cytology ; Transcription Factors/deficiency/*metabolism ; Tumor Suppressor Protein p53/metabolism ; Tyrosine/genetics/metabolism
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Reprogramming in vivo produces teratomas and iPS cells with totipotency features (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-09-13
    Description: Reprogramming of adult cells to generate induced pluripotent stem cells (iPS cells) has opened new therapeutic opportunities; however, little is known about the possibility of in vivo reprogramming within tissues. Here we show that transitory induction of the four factors Oct4, Sox2, Klf4 and c-Myc in mice results in teratomas emerging from multiple organs, implying that full reprogramming can occur in vivo. Analyses of the stomach, intestine, pancreas and kidney reveal groups of dedifferentiated cells that express the pluripotency marker NANOG, indicative of in situ reprogramming. By bone marrow transplantation, we demonstrate that haematopoietic cells can also be reprogrammed in vivo. Notably, reprogrammable mice present circulating iPS cells in the blood and, at the transcriptome level, these in vivo generated iPS cells are closer to embryonic stem cells (ES cells) than standard in vitro generated iPS cells. Moreover, in vivo iPS cells efficiently contribute to the trophectoderm lineage, suggesting that they achieve a more plastic or primitive state than ES cells. Finally, intraperitoneal injection of in vivo iPS cells generates embryo-like structures that express embryonic and extraembryonic markers. We conclude that reprogramming in vivo is feasible and confers totipotency features absent in standard iPS or ES cells. These discoveries could be relevant for future applications of reprogramming in regenerative medicine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abad, Maria -- Mosteiro, Lluc -- Pantoja, Cristina -- Canamero, Marta -- Rayon, Teresa -- Ors, Inmaculada -- Grana, Osvaldo -- Megias, Diego -- Dominguez, Orlando -- Martinez, Dolores -- Manzanares, Miguel -- Ortega, Sagrario -- Serrano, Manuel -- England -- Nature. 2013 Oct 17;502(7471):340-5. doi: 10.1038/nature12586. Epub 2013 Sep 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tumour Suppression Group, Spanish National Cancer Research Centre (CNIO), Madrid E-28029, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24025773" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Cells/cytology/metabolism ; Cell Dedifferentiation ; Cell Separation ; Cells, Cultured ; *Cellular Reprogramming/genetics ; Ectoderm/cytology ; Embryoid Bodies/cytology/metabolism ; Embryonic Stem Cells/cytology/metabolism ; Female ; Fibroblasts/cytology ; Gene Expression Profiling ; Induced Pluripotent Stem Cells/*cytology/metabolism ; Intestines/cytology ; Kidney/cytology ; Kruppel-Like Transcription Factors/genetics/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Octamer Transcription Factor-3/genetics/metabolism ; Organ Specificity ; Pancreas/cytology ; Proto-Oncogene Proteins c-myc/genetics/metabolism ; SOXB1 Transcription Factors/genetics/metabolism ; Stomach/cytology ; Teratoma/genetics/*metabolism/pathology ; Totipotent Stem Cells/*cytology/metabolism ; Transcriptome/genetics ; Trophoblasts/cytology
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  • 5
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    T-helper-1-cell cytokines drive cancer into senescence (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-02-05
    Description: Cancer control by adaptive immunity involves a number of defined death and clearance mechanisms. However, efficient inhibition of exponential cancer growth by T cells and interferon-gamma (IFN-gamma) requires additional undefined mechanisms that arrest cancer cell proliferation. Here we show that the combined action of the T-helper-1-cell cytokines IFN-gamma and tumour necrosis factor (TNF) directly induces permanent growth arrest in cancers. To safely separate senescence induced by tumour immunity from oncogene-induced senescence, we used a mouse model in which the Simian virus 40 large T antigen (Tag) expressed under the control of the rat insulin promoter creates tumours by attenuating p53- and Rb-mediated cell cycle control. When combined, IFN-gamma and TNF drive Tag-expressing cancers into senescence by inducing permanent growth arrest in G1/G0, activation of p16INK4a (also known as CDKN2A), and downstream Rb hypophosphorylation at serine 795. This cytokine-induced senescence strictly requires STAT1 and TNFR1 (also known as TNFRSF1A) signalling in addition to p16INK4a. In vivo, Tag-specific T-helper 1 cells permanently arrest Tag-expressing cancers by inducing IFN-gamma- and TNFR1-dependent senescence. Conversely, Tnfr1(-/-)Tag-expressing cancers resist cytokine-induced senescence and grow aggressively, even in TNFR1-expressing hosts. Finally, as IFN-gamma and TNF induce senescence in numerous murine and human cancers, this may be a general mechanism for arresting cancer progression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Braumuller, Heidi -- Wieder, Thomas -- Brenner, Ellen -- Assmann, Sonja -- Hahn, Matthias -- Alkhaled, Mohammed -- Schilbach, Karin -- Essmann, Frank -- Kneilling, Manfred -- Griessinger, Christoph -- Ranta, Felicia -- Ullrich, Susanne -- Mocikat, Ralph -- Braungart, Kilian -- Mehra, Tarun -- Fehrenbacher, Birgit -- Berdel, Julia -- Niessner, Heike -- Meier, Friedegund -- van den Broek, Maries -- Haring, Hans-Ulrich -- Handgretinger, Rupert -- Quintanilla-Martinez, Leticia -- Fend, Falko -- Pesic, Marina -- Bauer, Jurgen -- Zender, Lars -- Schaller, Martin -- Schulze-Osthoff, Klaus -- Rocken, Martin -- England -- Nature. 2013 Feb 21;494(7437):361-5. doi: 10.1038/nature11824. Epub 2013 Feb 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, Eberhard Karls University, Liebermeister Strasse 25, 72076 Tubingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23376950" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Polyomavirus Transforming/genetics/metabolism ; Cell Aging/*immunology ; Cell Cycle ; Cell Proliferation ; Cyclin-Dependent Kinase Inhibitor p16/deficiency/genetics/metabolism ; Cytokines/*immunology ; Disease Models, Animal ; Disease Progression ; Female ; Humans ; Interferon-gamma/immunology ; Male ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic ; Neoplasms/*immunology/*pathology ; Oncogenes/genetics ; Phosphoserine/metabolism ; Receptors, Tumor Necrosis Factor, Type I/metabolism ; Retinoblastoma Protein/chemistry/metabolism ; STAT1 Transcription Factor/metabolism ; Th1 Cells/*immunology ; Time Factors ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha/immunology ; Tumor Suppressor Protein p53/metabolism
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    DNA-damage-induced differentiation of leukaemic cells as an anti-cancer barrier (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-08-01
    Description: Self-renewal is the hallmark feature both of normal stem cells and cancer stem cells. Since the regenerative capacity of normal haematopoietic stem cells is limited by the accumulation of reactive oxygen species and DNA double-strand breaks, we speculated that DNA damage might also constrain leukaemic self-renewal and malignant haematopoiesis. Here we show that the histone methyl-transferase MLL4, a suppressor of B-cell lymphoma, is required for stem-cell activity and an aggressive form of acute myeloid leukaemia harbouring the MLL-AF9 oncogene. Deletion of MLL4 enhances myelopoiesis and myeloid differentiation of leukaemic blasts, which protects mice from death related to acute myeloid leukaemia. MLL4 exerts its function by regulating transcriptional programs associated with the antioxidant response. Addition of reactive oxygen species scavengers or ectopic expression of FOXO3 protects MLL4(-/-) MLL-AF9 cells from DNA damage and inhibits myeloid maturation. Similar to MLL4 deficiency, loss of ATM or BRCA1 sensitizes transformed cells to differentiation, suggesting that myeloid differentiation is promoted by loss of genome integrity. Indeed, we show that restriction-enzyme-induced double-strand breaks are sufficient to induce differentiation of MLL-AF9 blasts, which requires cyclin-dependent kinase inhibitor p21(Cip1) (Cdkn1a) activity. In summary, we have uncovered an unexpected tumour-promoting role of genome guardians in enforcing the oncogene-induced differentiation blockade in acute myeloid leukaemia.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4410707/" 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/PMC4410707/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Santos, Margarida A -- Faryabi, Robert B -- Ergen, Aysegul V -- Day, Amanda M -- Malhowski, Amy -- Canela, Andres -- Onozawa, Masahiro -- Lee, Ji-Eun -- Callen, Elsa -- Gutierrez-Martinez, Paula -- Chen, Hua-Tang -- Wong, Nancy -- Finkel, Nadia -- Deshpande, Aniruddha -- Sharrow, Susan -- Rossi, Derrick J -- Ito, Keisuke -- Ge, Kai -- Aplan, Peter D -- Armstrong, Scott A -- Nussenzweig, Andre -- CA140575/CA/NCI NIH HHS/ -- CA66996/CA/NCI NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- R00 CA139009/CA/NCI NIH HHS/ -- R01 DK098263/DK/NIDDK NIH HHS/ -- R01 DK100689/DK/NIDDK NIH HHS/ -- Intramural NIH HHS/ -- England -- Nature. 2014 Oct 2;514(7520):107-11. doi: 10.1038/nature13483. Epub 2014 Jul 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genome Integrity, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. ; 1] Laboratory of Genome Integrity, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA [2]. ; The Genetics Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. ; Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. ; 1] Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, Massachusetts 02115, USA [2] Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, Massachusetts 02138, USA. ; Human Oncology and Pathogenesis Program and Department of Pediatrics, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA. ; Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. ; Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research, Departments of Cell Biology and Medicine, Albert Einstein Cancer Center, Albert Einstein College of Medicine, Bronx, New York 10461, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25079327" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxia Telangiectasia Mutated Proteins/metabolism ; BRCA1 Protein/genetics/metabolism ; Cell Transformation, Neoplastic ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; DNA Breaks, Double-Stranded ; *DNA Damage ; DNA Repair ; Female ; Gene Expression Regulation, Neoplastic ; Genes, BRCA1 ; Hematopoietic Stem Cells/cytology/metabolism/pathology ; Histone-Lysine N-Methyltransferase/deficiency/genetics/metabolism ; Leukemia, Myeloid, Acute/*enzymology/*pathology ; Male ; Mice ; *Myelopoiesis ; Oncogene Proteins, Fusion/genetics/metabolism ; Reactive Oxygen Species/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Insights into hominid evolution from the gorilla genome sequence (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-03-09
    Description: Gorillas are humans' closest living relatives after chimpanzees, and are of comparable importance for the study of human origins and evolution. Here we present the assembly and analysis of a genome sequence for the western lowland gorilla, and compare the whole genomes of all extant great ape genera. We propose a synthesis of genetic and fossil evidence consistent with placing the human-chimpanzee and human-chimpanzee-gorilla speciation events at approximately 6 and 10 million years ago. In 30% of the genome, gorilla is closer to human or chimpanzee than the latter are to each other; this is rarer around coding genes, indicating pervasive selection throughout great ape evolution, and has functional consequences in gene expression. A comparison of protein coding genes reveals approximately 500 genes showing accelerated evolution on each of the gorilla, human and chimpanzee lineages, and evidence for parallel acceleration, particularly of genes involved in hearing. We also compare the western and eastern gorilla species, estimating an average sequence divergence time 1.75 million years ago, but with evidence for more recent genetic exchange and a population bottleneck in the eastern species. The use of the genome sequence in these and future analyses will promote a deeper understanding of great ape biology and evolution.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3303130/" 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/PMC3303130/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scally, Aylwyn -- Dutheil, Julien Y -- Hillier, LaDeana W -- Jordan, Gregory E -- Goodhead, Ian -- Herrero, Javier -- Hobolth, Asger -- Lappalainen, Tuuli -- Mailund, Thomas -- Marques-Bonet, Tomas -- McCarthy, Shane -- Montgomery, Stephen H -- Schwalie, Petra C -- Tang, Y Amy -- Ward, Michelle C -- Xue, Yali -- Yngvadottir, Bryndis -- Alkan, Can -- Andersen, Lars N -- Ayub, Qasim -- Ball, Edward V -- Beal, Kathryn -- Bradley, Brenda J -- Chen, Yuan -- Clee, Chris M -- Fitzgerald, Stephen -- Graves, Tina A -- Gu, Yong -- Heath, Paul -- Heger, Andreas -- Karakoc, Emre -- Kolb-Kokocinski, Anja -- Laird, Gavin K -- Lunter, Gerton -- Meader, Stephen -- Mort, Matthew -- Mullikin, James C -- Munch, Kasper -- O'Connor, Timothy D -- Phillips, Andrew D -- Prado-Martinez, Javier -- Rogers, Anthony S -- Sajjadian, Saba -- Schmidt, Dominic -- Shaw, Katy -- Simpson, Jared T -- Stenson, Peter D -- Turner, Daniel J -- Vigilant, Linda -- Vilella, Albert J -- Whitener, Weldon -- Zhu, Baoli -- Cooper, David N -- de Jong, Pieter -- Dermitzakis, Emmanouil T -- Eichler, Evan E -- Flicek, Paul -- Goldman, Nick -- Mundy, Nicholas I -- Ning, Zemin -- Odom, Duncan T -- Ponting, Chris P -- Quail, Michael A -- Ryder, Oliver A -- Searle, Stephen M -- Warren, Wesley C -- Wilson, Richard K -- Schierup, Mikkel H -- Rogers, Jane -- Tyler-Smith, Chris -- Durbin, Richard -- 062023/Wellcome Trust/United Kingdom -- 075491/Z/04/Wellcome Trust/United Kingdom -- 077009/Wellcome Trust/United Kingdom -- 077192/Wellcome Trust/United Kingdom -- 077198/Wellcome Trust/United Kingdom -- 089066/Wellcome Trust/United Kingdom -- 090532/Wellcome Trust/United Kingdom -- 095908/Wellcome Trust/United Kingdom -- 15603/Cancer Research UK/United Kingdom -- 202218/European Research Council/International -- A15603/Cancer Research UK/United Kingdom -- G0501331/Medical Research Council/United Kingdom -- G0701805/Medical Research Council/United Kingdom -- HG002385/HG/NHGRI NIH HHS/ -- U54 HG003079/HG/NHGRI NIH HHS/ -- WT062023/Wellcome Trust/United Kingdom -- WT077009/Wellcome Trust/United Kingdom -- WT077192/Wellcome Trust/United Kingdom -- WT077198/Wellcome Trust/United Kingdom -- WT089066/Wellcome Trust/United Kingdom -- Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- England -- Nature. 2012 Mar 7;483(7388):169-75. doi: 10.1038/nature10842.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22398555" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Evolution, Molecular ; Female ; Gene Expression Regulation ; *Genetic Speciation ; Genetic Variation/genetics ; Genome/*genetics ; Genomics ; Gorilla gorilla/*genetics ; Humans ; Macaca mulatta/genetics ; Molecular Sequence Data ; Pan troglodytes/genetics ; Phylogeny ; Pongo/genetics ; Proteins/genetics ; Sequence Alignment ; Species Specificity ; Transcription, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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