Male-to-female sex reversal in M33 mutant mice

Yuko Katoh-Fukui (), Reiko Tsuchiya, Toshihiko Shiroishi, Yoko Nakahara, Naoko Hashimoto, Kousei Noguchi and Toru Higashinakagawa
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Yuko Katoh-Fukui: Mitsubishi Kasei Institute of Life Sciences
Reiko Tsuchiya: Mitsubishi Kasei Institute of Life Sciences
Toshihiko Shiroishi: Mammalian Genetics Laboratory, National Institute of Genetics
Yoko Nakahara: Mitsubishi Kasei Institute of Life Sciences
Naoko Hashimoto: Mitsubishi Kasei Institute of Life Sciences
Kousei Noguchi: Waseda University
Toru Higashinakagawa: Waseda University

Nature, 1998, vol. 393, issue 6686, 688-692

Abstract: Abstract Polycomb genes in Drosophila maintain the repressed state of homeotic and other developmentally regulated genes1,2,3,4 by mediating changes in higher-order chromatin structure5,6,7. M33, a mouse homologue of Polycomb, was isolated by means of the structural similarity of its chromodomain8. The fifth exon of M33 contains a region of homology shared by Drosophila and Xenopus8,9. In Drosophila, its deletion results in the loss of Polycomb function10. Here we have disrupted M33 in mice by inserting a poly(A) capture-type neor 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 gene11, 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.

Date: 1998
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DOI: 10.1038/31482

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