Male-to-female sex reversal in M33 mutant mice View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1998-06

AUTHORS

Y Katoh-Fukui, R Tsuchiya, T Shiroishi, Y Nakahara, N Hashimoto, K Noguchi, T Higashinakagawa

ABSTRACT

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. More... »

PAGES

688-692

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/31482

DOI

http://dx.doi.org/10.1038/31482

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1007201071

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9641679


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