a genetic basis for a postmeiotic x versus y chromosome intragenomic conflict in the mousepostmeiotic x和y染色体的遗传基础老鼠基因内的冲突.pdfVIP

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a genetic basis for a postmeiotic x versus y chromosome intragenomic conflict in the mousepostmeiotic x和y染色体的遗传基础老鼠基因内的冲突.pdf

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a genetic basis for a postmeiotic x versus y chromosome intragenomic conflict in the mousepostmeiotic x和y染色体的遗传基础老鼠基因内的冲突

A Genetic Basis for a Postmeiotic X Versus Y Chromosome Intragenomic Conflict in the Mouse 1,2,3 4 5 4 1,2,3 Julie Cocquet *, Peter J. I. Ellis , Shantha K. Mahadevaiah , Nabeel A. Affara , Daniel Vaiman , Paul S. Burgoyne5 ´ ´ 1 Inserm, U1016, Institut Cochin, Paris, France, 2 CNRS, UMR8104, Paris, France, 3 Universite Paris Descartes, Sorbonne Paris Cite, Paris, France, 4 Department of Pathology, Mammalian Molecular Genetics Group, University of Cambridge, Cambridge, United Kingdom, 5 Division of Stem Cell Biology and Developmental Genetics, MRC National Institute for Medical Research, London, United Kingdom Abstract Intragenomic conflicts arise when a genetic element favours its own transmission to the detriment of others. Conflicts over sex chromosome transmission are expected to have influenced genome structure, gene regulation, and speciation. In the mouse, the existence of an intragenomic conflict between X- and Y-linked multicopy genes has long been suggested but never demonstrated. The Y-encoded multicopy gene Sly has been shown to have a predominant role in the epigenetic repression of post meiotic sex chromatin (PMSC) and, as such, represses X and Y genes, among which are its X-linked homologs Slx and Slxl1. Here, we produced mice that are deficient for both Sly and Slx/Slxl1 and observed that Slx/Slxl1 has an opposite role to that of Sly, in that it stimulates XY gene expression in spermatids. Slx/Slxl1 deficiency rescues the sperm differentiation defects and near sterility caused by Sly deficiency and vice versa. Slx/Slxl1