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  • *Symbiosis  (1)
  • Behavior, Animal  (1)
  • Nature Publishing Group (NPG)  (2)
  • American Chemical Society (ACS)
  • Cell Press
  • Geological Society London
  • 2010-2014  (2)
Collection
Publisher
  • Nature Publishing Group (NPG)  (2)
  • American Chemical Society (ACS)
  • Cell Press
  • Geological Society London
Years
  • 2010-2014  (2)
Year
  • 1
    Publication Date: 2011-11-18
    Description: Legumes (Fabaceae or Leguminosae) are unique among cultivated plants for their ability to carry out endosymbiotic nitrogen fixation with rhizobial bacteria, a process that takes place in a specialized structure known as the nodule. Legumes belong to one of the two main groups of eurosids, the Fabidae, which includes most species capable of endosymbiotic nitrogen fixation. Legumes comprise several evolutionary lineages derived from a common ancestor 60 million years ago (Myr ago). Papilionoids are the largest clade, dating nearly to the origin of legumes and containing most cultivated species. Medicago truncatula is a long-established model for the study of legume biology. Here we describe the draft sequence of the M. truncatula euchromatin based on a recently completed BAC assembly supplemented with Illumina shotgun sequence, together capturing approximately 94% of all M. truncatula genes. A whole-genome duplication (WGD) approximately 58 Myr ago had a major role in shaping the M. truncatula genome and thereby contributed to the evolution of endosymbiotic nitrogen fixation. Subsequent to the WGD, the M. truncatula genome experienced higher levels of rearrangement than two other sequenced legumes, Glycine max and Lotus japonicus. M. truncatula is a close relative of alfalfa (Medicago sativa), a widely cultivated crop with limited genomics tools and complex autotetraploid genetics. As such, the M. truncatula genome sequence provides significant opportunities to expand alfalfa's genomic toolbox.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3272368/" 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/PMC3272368/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Young, Nevin D -- Debelle, Frederic -- Oldroyd, Giles E D -- Geurts, Rene -- Cannon, Steven B -- Udvardi, Michael K -- Benedito, Vagner A -- Mayer, Klaus F X -- Gouzy, Jerome -- Schoof, Heiko -- Van de Peer, Yves -- Proost, Sebastian -- Cook, Douglas R -- Meyers, Blake C -- Spannagl, Manuel -- Cheung, Foo -- De Mita, Stephane -- Krishnakumar, Vivek -- Gundlach, Heidrun -- Zhou, Shiguo -- Mudge, Joann -- Bharti, Arvind K -- Murray, Jeremy D -- Naoumkina, Marina A -- Rosen, Benjamin -- Silverstein, Kevin A T -- Tang, Haibao -- Rombauts, Stephane -- Zhao, Patrick X -- Zhou, Peng -- Barbe, Valerie -- Bardou, Philippe -- Bechner, Michael -- Bellec, Arnaud -- Berger, Anne -- Berges, Helene -- Bidwell, Shelby -- Bisseling, Ton -- Choisne, Nathalie -- Couloux, Arnaud -- Denny, Roxanne -- Deshpande, Shweta -- Dai, Xinbin -- Doyle, Jeff J -- Dudez, Anne-Marie -- Farmer, Andrew D -- Fouteau, Stephanie -- Franken, Carolien -- Gibelin, Chrystel -- Gish, John -- Goldstein, Steven -- Gonzalez, Alvaro J -- Green, Pamela J -- Hallab, Asis -- Hartog, Marijke -- Hua, Axin -- Humphray, Sean J -- Jeong, Dong-Hoon -- Jing, Yi -- Jocker, Anika -- Kenton, Steve M -- Kim, Dong-Jin -- Klee, Kathrin -- Lai, Hongshing -- Lang, Chunting -- Lin, Shaoping -- Macmil, Simone L -- Magdelenat, Ghislaine -- Matthews, Lucy -- McCorrison, Jamison -- Monaghan, Erin L -- Mun, Jeong-Hwan -- Najar, Fares Z -- Nicholson, Christine -- Noirot, Celine -- O'Bleness, Majesta -- Paule, Charles R -- Poulain, Julie -- Prion, Florent -- Qin, Baifang -- Qu, Chunmei -- Retzel, Ernest F -- Riddle, Claire -- Sallet, Erika -- Samain, Sylvie -- Samson, Nicolas -- Sanders, Iryna -- Saurat, Olivier -- Scarpelli, Claude -- Schiex, Thomas -- Segurens, Beatrice -- Severin, Andrew J -- Sherrier, D Janine -- Shi, Ruihua -- Sims, Sarah -- Singer, Susan R -- Sinharoy, Senjuti -- Sterck, Lieven -- Viollet, Agnes -- Wang, Bing-Bing -- Wang, Keqin -- Wang, Mingyi -- Wang, Xiaohong -- Warfsmann, Jens -- Weissenbach, Jean -- White, Doug D -- White, Jim D -- Wiley, Graham B -- Wincker, Patrick -- Xing, Yanbo -- Yang, Limei -- Yao, Ziyun -- Ying, Fu -- Zhai, Jixian -- Zhou, Liping -- Zuber, Antoine -- Denarie, Jean -- Dixon, Richard A -- May, Gregory D -- Schwartz, David C -- Rogers, Jane -- Quetier, Francis -- Town, Christopher D -- Roe, Bruce A -- BB/G023832/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBS/B/11524/Biotechnology and Biological Sciences Research Council/United Kingdom -- England -- Nature. 2011 Nov 16;480(7378):520-4. doi: 10.1038/nature10625.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Pathology, University of Minnesota, St Paul, Minnesota 55108, USA. neviny@umn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22089132" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; *Genome, Plant ; Medicago truncatula/*genetics/*microbiology ; Molecular Sequence Data ; Nitrogen Fixation/genetics ; Rhizobium/*physiology ; Soybeans/genetics ; *Symbiosis ; Synteny ; Vitis/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2011-07-01
    Description: Rett's syndrome (RTT) is an X-chromosome-linked autism spectrum disorder caused by loss of function of the transcription factor methyl-CpG-binding protein 2 (MeCP2). Although MeCP2 is expressed in most tissues, loss of MeCP2 expression results primarily in neurological symptoms. Earlier studies suggested the idea that RTT is due exclusively to loss of MeCP2 function in neurons. Although defective neurons clearly underlie the aberrant behaviours, we and others showed recently that the loss of MECP2 from glia negatively influences neurons in a non-cell-autonomous fashion. Here we show that in globally MeCP2-deficient mice, re-expression of Mecp2 preferentially in astrocytes significantly improved locomotion and anxiety levels, restored respiratory abnormalities to a normal pattern, and greatly prolonged lifespan compared to globally null mice. Furthermore, restoration of MeCP2 in the mutant astrocytes exerted a non-cell-autonomous positive effect on mutant neurons in vivo, restoring normal dendritic morphology and increasing levels of the excitatory glutamate transporter VGLUT1. Our study shows that glia, like neurons, are integral components of the neuropathology of RTT, and supports the targeting of glia as a strategy for improving the associated symptoms.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3268776/" 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/PMC3268776/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lioy, Daniel T -- Garg, Saurabh K -- Monaghan, Caitlin E -- Raber, Jacob -- Foust, Kevin D -- Kaspar, Brian K -- Hirrlinger, Petra G -- Kirchhoff, Frank -- Bissonnette, John M -- Ballas, Nurit -- Mandel, Gail -- P30 NS061800/NS/NINDS NIH HHS/ -- R01 HD056503/HD/NICHD NIH HHS/ -- R01 HD056503-03/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Jun 29;475(7357):497-500. doi: 10.1038/nature10214.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute, Oregon Health and Science University, Portland, Oregon 97239, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21716289" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anxiety/metabolism ; Astrocytes/metabolism ; Behavior, Animal ; Disease Progression ; Female ; Gene Expression Regulation ; Male ; Methyl-CpG-Binding Protein 2/deficiency/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Motor Activity ; Neuroglia/*metabolism/pathology ; Neurons/metabolism ; Rett Syndrome/*genetics/*metabolism/physiopathology ; Vesicular Glutamate Transport Protein 1/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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