ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • *Gene Expression Regulation
  • American Association for the Advancement of Science (AAAS)  (2)
Collection
Publisher
  • American Association for the Advancement of Science (AAAS)  (2)
Years
  • 1
    Publication Date: 2003-11-01
    Description: Mutations in MeCP2, which encodes a protein that has been proposed to function as a global transcriptional repressor, are the cause of Rett syndrome (RT T), an X-linked progressive neurological disorder. Although the selective inactivation of MeCP2 in neurons is sufficient to confer a Rett-like phenotype in mice, the specific functions of MeCP2 in postmitotic neurons are not known. We find that MeCP2 binds selectively to BDNF promoter III and functions to repress expression of the BDNF gene. Membrane depolarization triggers the calcium-dependent phosphorylation and release of MeCP2 from BDNF promoter III, thereby facilitating transcription. These studies indicate that MeCP2 plays a key role in the control of neuronal activity-dependent gene regulation and suggest that the deregulation of this process may underlie the pathology of RT T.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Wen G -- Chang, Qiang -- Lin, Yingxi -- Meissner, Alexander -- West, Anne E -- Griffith, Eric C -- Jaenisch, Rudolf -- Greenberg, Michael E -- HD 18655/HD/NICHD NIH HHS/ -- NS28829/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 31;302(5646):885-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14593183" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain-Derived Neurotrophic Factor/*genetics ; Calcium/*metabolism ; Cell Membrane/physiology ; Cells, Cultured ; *Chromosomal Proteins, Non-Histone ; Cloning, Molecular ; CpG Islands ; DNA Methylation ; DNA-Binding Proteins/*metabolism ; Electrophoretic Mobility Shift Assay ; *Gene Expression Regulation ; Gene Silencing ; Histones/metabolism ; Methyl-CpG-Binding Protein 2 ; Methylation ; Mice ; Mice, Knockout ; Neurons/metabolism/physiology ; Phosphorylation ; Potassium Chloride/pharmacology ; Precipitin Tests ; Promoter Regions, Genetic ; Rats ; *Repressor Proteins ; Rett Syndrome/genetics ; *Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 2
    Publication Date: 2015-11-21
    Description: The DNA-binding protein PRDM9 has a critical role in specifying meiotic recombination hotspots in mice and apes, but it appears to be absent from other vertebrate species, including birds. To study the evolution and determinants of recombination in species lacking the gene that encodes PRDM9, we inferred fine-scale genetic maps from population resequencing data for two bird species: the zebra finch, Taeniopygia guttata, and the long-tailed finch, Poephila acuticauda. We found that both species have recombination hotspots, which are enriched near functional genomic elements. Unlike in mice and apes, most hotspots are shared between the two species, and their conservation seems to extend over tens of millions of years. These observations suggest that in the absence of PRDM9, recombination targets functional features that both enable access to the genome and constrain its evolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Singhal, Sonal -- Leffler, Ellen M -- Sannareddy, Keerthi -- Turner, Isaac -- Venn, Oliver -- Hooper, Daniel M -- Strand, Alva I -- Li, Qiye -- Raney, Brian -- Balakrishnan, Christopher N -- Griffith, Simon C -- McVean, Gil -- Przeworski, Molly -- 086786/Z/08/Z/Wellcome Trust/United Kingdom -- 090532/Z/09/Z/Wellcome Trust/United Kingdom -- 100956/Wellcome Trust/United Kingdom -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Nov 20;350(6263):928-32. doi: 10.1126/science.aad0843.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Columbia University, New York, NY 10027, USA. Department of Systems Biology, Columbia University, New York, NY 10032, USA. sonal.singhal1@gmail.com molly.przew@gmail.com. ; Department of Human Genetics, University of Chicago, Chicago, IL 60637, USA. Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX3 7BN, UK. ; Department of Human Genetics, University of Chicago, Chicago, IL 60637, USA. ; Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX3 7BN, UK. ; Committee on Evolutionary Biology, University of Chicago, Chicago, IL 60637, USA. ; Department of Biological Sciences, Columbia University, New York, NY 10027, USA. ; China National Genebank, BGI-Shenzhen, Shenzhen 518083, China. ; Center for Biomolecular Science and Engineering, University of California-Santa Cruz, Santa Cruz, CA 95064, USA. ; Department of Biology, East Carolina University, Greenville, NC 27858, USA. ; Department of Biological Sciences, Macquarie University, Sydney, NSW 2109, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26586757" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; *Evolution, Molecular ; Finches/*genetics ; *Gene Expression Regulation ; Genome ; *Recombination, Genetic ; Repressor Proteins/*genetics ; Species Specificity
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...