Linked Life Data

16580996

Source:http://linkedlifedata.com/resource/pubmed/id/16580996

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-4-3
pubmed:abstractText
Transcriptional silencing of the sex chromosomes during male meiosis (MSCI) is conserved among organisms with limited sex chromosome synapsis, including mammals. Since the 1990s the prevailing view has been that MSCI in mammals is transient, with sex chromosome reactivation occurring as cells exit meiosis. Recently, we found that any chromosome region unsynapsed during pachytene of male and female mouse meiosis is subject to transcriptional silencing (MSUC), and we hypothesized that MSCI is an inevitable consequence of this more general meiotic silencing mechanism. Here, we provide direct evidence that asynapsis does indeed drive MSCI. We also show that a substantial degree of transcriptional repression of the sex chromosomes is retained postmeiotically, and we provide evidence that this postmeiotic repression is a downstream consequence of MSCI/MSUC. While this postmeiotic repression occurs after the loss of MSUC-related proteins at the end of prophase, other histone modifications associated with transcriptional repression have by then become established.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1534-5807
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
521-9
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Pachytene asynapsis drives meiotic sex chromosome inactivation and leads to substantial postmeiotic repression in spermatids.
pubmed:affiliation
Division of Developmental Genetics and Stem Cell Research, MRC National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, United Kingdom. jturner@nimr.nrc.ac.uk
pubmed:publicationType
Journal Article