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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6686
pubmed:dateCreated
1998-7-1
pubmed:abstractText
Polycomb genes in Drosophila maintain the repressed state of homeotic and other developmentally regulated genes by mediating changes in higher-order chromatin structure. M33, a mouse homologue of Polycomb, was isolated by means of the structural similarity of its chromodomain. The fifth exon of M33 contains a region of homology shared by Drosophila and Xenopus. In Drosophila, its deletion results in the loss of Polycomb function. Here we have disrupted M33 in mice by inserting a poly(A) capture-type neo(r) targeting vector into its fifth exon. More than half of the resultant M33cterm/M33cterm mutant mice died before weaning, and survivors showed male-to-female sex reversal. Formation of genital ridges was retarded in both XX and XY M33cterm/M33cterm embryos. Gonadal growth defects appeared near the time of expression of the Y-chromosome-specific Sry gene, suggesting that M33 deficiency may cause sex reversal by interfering with steps upstream of Sry. M33cterm/M33cterm mice may be a valuable model in which to test opposing views regarding sex determination.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0028-0836
pubmed:author
pubmed:issnType
Print
pubmed:day
18
pubmed:volume
393
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
688-92
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Male-to-female sex reversal in M33 mutant mice.
pubmed:affiliation
Mitsubishi Kasei Institute of Life Sciences, Machida, Tokyo, Japan. kan@libra.ls.mkagaku.co.jp
pubmed:publicationType
Journal Article