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  • Gene Expression Regulation  (2)
  • Nature Publishing Group (NPG)  (2)
  • 1
    Publication Date: 2008-02-15
    Description: Choanoflagellates are the closest known relatives of metazoans. To discover potential molecular mechanisms underlying the evolution of metazoan multicellularity, we sequenced and analysed the genome of the unicellular choanoflagellate Monosiga brevicollis. The genome contains approximately 9,200 intron-rich genes, including a number that encode cell adhesion and signalling protein domains that are otherwise restricted to metazoans. Here we show that the physical linkages among protein domains often differ between M. brevicollis and metazoans, suggesting that abundant domain shuffling followed the separation of the choanoflagellate and metazoan lineages. The completion of the M. brevicollis genome allows us to reconstruct with increasing resolution the genomic changes that accompanied the origin of metazoans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2562698/" 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/PMC2562698/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉King, Nicole -- Westbrook, M Jody -- Young, Susan L -- Kuo, Alan -- Abedin, Monika -- Chapman, Jarrod -- Fairclough, Stephen -- Hellsten, Uffe -- Isogai, Yoh -- Letunic, Ivica -- Marr, Michael -- Pincus, David -- Putnam, Nicholas -- Rokas, Antonis -- Wright, Kevin J -- Zuzow, Richard -- Dirks, William -- Good, Matthew -- Goodstein, David -- Lemons, Derek -- Li, Wanqing -- Lyons, Jessica B -- Morris, Andrea -- Nichols, Scott -- Richter, Daniel J -- Salamov, Asaf -- Sequencing, J G I -- Bork, Peer -- Lim, Wendell A -- Manning, Gerard -- Miller, W Todd -- McGinnis, William -- Shapiro, Harris -- Tjian, Robert -- Grigoriev, Igor V -- Rokhsar, Daniel -- R01 CA058530/CA/NCI NIH HHS/ -- R01 CA058530-14/CA/NCI NIH HHS/ -- R01 GM077197/GM/NIGMS NIH HHS/ -- R01 HG004164/HG/NHGRI NIH HHS/ -- R01 HG004164-01/HG/NHGRI NIH HHS/ -- R37 HD028315/HD/NICHD NIH HHS/ -- England -- Nature. 2008 Feb 14;451(7180):783-8. doi: 10.1038/nature06617.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology and the Center for Integrative Genomics, University of California, Berkeley, California 94720, USA. nking@berkeley.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18273011" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Adhesion ; Conserved Sequence ; Eukaryotic Cells/classification/cytology/*metabolism ; Evolution, Molecular ; Extracellular Matrix/metabolism ; Gene Expression Regulation ; Genetic Speciation ; Genome/*genetics ; Hedgehog Proteins/chemistry/genetics ; Humans ; Introns/genetics ; Phosphotyrosine/metabolism ; *Phylogeny ; Protein Structure, Tertiary/genetics ; Receptors, Notch/chemistry/genetics ; Signal Transduction/genetics ; Transcription Factors/genetics/metabolism ; Transcription, Genetic
    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: 2013-09-13
    Description: Down's syndrome results from full or partial trisomy of chromosome 21. However, the consequences of the underlying gene-dosage imbalance on adult tissues remain poorly understood. Here we show that in Ts65Dn mice, which are trisomic for 132 genes homologous to genes on human chromosome 21, triplication of Usp16 reduces the self-renewal of haematopoietic stem cells and the expansion of mammary epithelial cells, neural progenitors and fibroblasts. In addition, Usp16 is associated with decreased ubiquitination of Cdkn2a and accelerated senescence in Ts65Dn fibroblasts. Usp16 can remove ubiquitin from histone H2A on lysine 119, a critical mark for the maintenance of multiple somatic tissues. Downregulation of Usp16, either by mutation of a single normal Usp16 allele or by short interfering RNAs, largely rescues all of these defects. Furthermore, in human tissues overexpression of USP16 reduces the expansion of normal fibroblasts and postnatal neural progenitors, whereas downregulation of USP16 partially rescues the proliferation defects of Down's syndrome fibroblasts. Taken together, these results suggest that USP16 has an important role in antagonizing the self-renewal and/or senescence pathways in Down's syndrome and could serve as an attractive target to ameliorate some of the associated pathologies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3816928/" 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/PMC3816928/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adorno, Maddalena -- Sikandar, Shaheen -- Mitra, Siddhartha S -- Kuo, Angera -- Nicolis Di Robilant, Benedetta -- Haro-Acosta, Veronica -- Ouadah, Youcef -- Quarta, Marco -- Rodriguez, Jacqueline -- Qian, Dalong -- Reddy, Vadiyala M -- Cheshier, Samuel -- Garner, Craig C -- Clarke, Michael F -- CA100225/CA/NCI NIH HHS/ -- CA154209/CA/NCI NIH HHS/ -- R01 CA100225/CA/NCI NIH HHS/ -- R01 CA104987/CA/NCI NIH HHS/ -- T32 CA009302/CA/NCI NIH HHS/ -- U01 CA154209/CA/NCI NIH HHS/ -- England -- Nature. 2013 Sep 19;501(7467):380-4. doi: 10.1038/nature12530. Epub 2013 Sep 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24025767" target="_blank"〉PubMed〈/a〉
    Keywords: Adult Stem Cells/metabolism/pathology ; Animals ; Cell Aging ; Cell Proliferation ; Chromosomes, Human, Pair 21/genetics ; Cyclin-Dependent Kinase Inhibitor p16/metabolism ; Disease Models, Animal ; Down Syndrome/genetics/*metabolism/*pathology ; Epithelium/metabolism ; Female ; Fibroblasts/cytology/metabolism/pathology ; Gene Dosage ; Gene Expression Regulation ; Hematopoietic Stem Cells/cytology/pathology ; Humans ; Mammary Glands, Animal/cytology/metabolism ; Mice ; Molecular Targeted Therapy ; Neural Stem Cells/*metabolism/*pathology ; Trisomy/genetics ; Ubiquitin Thiolesterase/genetics/*metabolism ; Ubiquitination
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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