The multicopy gene Sly represses the sex chromosomes in the male mouse germline after meiosis.

Studies of mice with Y chromosome long arm deficiencies suggest that the male-specific region (MSYq) encodes information required for sperm differentiation and postmeiotic sex chromatin repression (PSCR). Several genes have been identified on MSYq, but because they are present in more than 40 copies...

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Autores principales: Julie Cocquet, Peter J I Ellis, Yasuhiro Yamauchi, Shantha K Mahadevaiah, Nabeel A Affara, Monika A Ward, Paul S Burgoyne
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Publicado: Public Library of Science (PLoS) 2009
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spelling oai:doaj.org-article:fb880ebd02244839baabfc823f4e2d472021-11-25T05:34:29ZThe multicopy gene Sly represses the sex chromosomes in the male mouse germline after meiosis.1544-91731545-788510.1371/journal.pbio.1000244https://doaj.org/article/fb880ebd02244839baabfc823f4e2d472009-11-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19918361/?tool=EBIhttps://doaj.org/toc/1544-9173https://doaj.org/toc/1545-7885Studies of mice with Y chromosome long arm deficiencies suggest that the male-specific region (MSYq) encodes information required for sperm differentiation and postmeiotic sex chromatin repression (PSCR). Several genes have been identified on MSYq, but because they are present in more than 40 copies each, their functions cannot be investigated using traditional gene targeting. Here, we generate transgenic mice producing small interfering RNAs that specifically target the transcripts of the MSYq-encoded multicopy gene Sly (Sycp3-like Y-linked). Microarray analyses performed on these Sly-deficient males and on MSYq-deficient males show a remarkable up-regulation of sex chromosome genes in spermatids. SLY protein colocalizes with the X and Y chromatin in spermatids of normal males, and Sly deficiency leads to defective repressive marks on the sex chromatin, such as reduced levels of the heterochromatin protein CBX1 and of histone H3 methylated at lysine 9. Sly-deficient mice, just like MSYq-deficient mice, have severe impairment of sperm differentiation and are near sterile. We propose that their spermiogenesis phenotype is a consequence of the change in spermatid gene expression following Sly deficiency. To our knowledge, this is the first successful targeted disruption of the function of a multicopy gene (or of any Y gene). It shows that SLY has a predominant role in PSCR, either via direct interaction with the spermatid sex chromatin or via interaction with sex chromatin protein partners. Sly deficiency is the major underlying cause of the spectrum of anomalies identified 17 y ago in MSYq-deficient males. Our results also suggest that the expansion of sex-linked spermatid-expressed genes in mouse is a consequence of the enhancement of PSCR that accompanies Sly amplification.Julie CocquetPeter J I EllisYasuhiro YamauchiShantha K MahadevaiahNabeel A AffaraMonika A WardPaul S BurgoynePublic Library of Science (PLoS)articleBiology (General)QH301-705.5ENPLoS Biology, Vol 7, Iss 11, p e1000244 (2009)
institution DOAJ
collection DOAJ
language EN
topic Biology (General)
QH301-705.5
spellingShingle Biology (General)
QH301-705.5
Julie Cocquet
Peter J I Ellis
Yasuhiro Yamauchi
Shantha K Mahadevaiah
Nabeel A Affara
Monika A Ward
Paul S Burgoyne
The multicopy gene Sly represses the sex chromosomes in the male mouse germline after meiosis.
description Studies of mice with Y chromosome long arm deficiencies suggest that the male-specific region (MSYq) encodes information required for sperm differentiation and postmeiotic sex chromatin repression (PSCR). Several genes have been identified on MSYq, but because they are present in more than 40 copies each, their functions cannot be investigated using traditional gene targeting. Here, we generate transgenic mice producing small interfering RNAs that specifically target the transcripts of the MSYq-encoded multicopy gene Sly (Sycp3-like Y-linked). Microarray analyses performed on these Sly-deficient males and on MSYq-deficient males show a remarkable up-regulation of sex chromosome genes in spermatids. SLY protein colocalizes with the X and Y chromatin in spermatids of normal males, and Sly deficiency leads to defective repressive marks on the sex chromatin, such as reduced levels of the heterochromatin protein CBX1 and of histone H3 methylated at lysine 9. Sly-deficient mice, just like MSYq-deficient mice, have severe impairment of sperm differentiation and are near sterile. We propose that their spermiogenesis phenotype is a consequence of the change in spermatid gene expression following Sly deficiency. To our knowledge, this is the first successful targeted disruption of the function of a multicopy gene (or of any Y gene). It shows that SLY has a predominant role in PSCR, either via direct interaction with the spermatid sex chromatin or via interaction with sex chromatin protein partners. Sly deficiency is the major underlying cause of the spectrum of anomalies identified 17 y ago in MSYq-deficient males. Our results also suggest that the expansion of sex-linked spermatid-expressed genes in mouse is a consequence of the enhancement of PSCR that accompanies Sly amplification.
format article
author Julie Cocquet
Peter J I Ellis
Yasuhiro Yamauchi
Shantha K Mahadevaiah
Nabeel A Affara
Monika A Ward
Paul S Burgoyne
author_facet Julie Cocquet
Peter J I Ellis
Yasuhiro Yamauchi
Shantha K Mahadevaiah
Nabeel A Affara
Monika A Ward
Paul S Burgoyne
author_sort Julie Cocquet
title The multicopy gene Sly represses the sex chromosomes in the male mouse germline after meiosis.
title_short The multicopy gene Sly represses the sex chromosomes in the male mouse germline after meiosis.
title_full The multicopy gene Sly represses the sex chromosomes in the male mouse germline after meiosis.
title_fullStr The multicopy gene Sly represses the sex chromosomes in the male mouse germline after meiosis.
title_full_unstemmed The multicopy gene Sly represses the sex chromosomes in the male mouse germline after meiosis.
title_sort multicopy gene sly represses the sex chromosomes in the male mouse germline after meiosis.
publisher Public Library of Science (PLoS)
publishDate 2009
url https://doaj.org/article/fb880ebd02244839baabfc823f4e2d47
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