Human Molecular Genetics Advance Access originally published online on August 8, 2005
Human Molecular Genetics 2005 14(18):2705-2715; doi:10.1093/hmg/ddi304
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Deletions on mouse Yq lead to upregulation of multiple X- and Y-linked transcripts in spermatids
1Department of Pathology, Mammalian Molecular Genetics Group, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK, 2RC Centre of Excellence in Biotechnology and Development, Monash Institute for Medical Research, Monash University, Clayton, Melbourne, Victoria 3168, Australia and 3Division of Stem Cell Research and Developmental Genetics, MRC National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, UK
* To whom correspondence should be addressed. Tel: +44 01223 333700; Fax: +44 01223 333346; Email: na{at}mole.bio.cam.ac.uk
Received June 24, 2005; Revised July 22, 2005; Accepted August 2, 2005
Deletions on the mouse Y-chromosome long arm (MSYq) lead to teratozoospermia and in severe cases to infertility. We find that the downstream transcriptional changes in the testis resulting from the loss of MSYq-encoded transcripts involve upregulation of multiple X- and Y-linked spermatid-expressed genes, but not related autosomal genes. Therefore, this indicates that in normal males, there is a specific repression of X and Y (gonosomal) transcription in post-meiotic cells, which depends on MSYq-encoded transcripts. Together with the known sex ratio skew in favour of females in the offspring of fertile MSYqdel males, this strongly suggests the existence of an intragenomic conflict between X- and Y-linked genes. Two potential antagonists in this conflict are the X-linked multicopy gene Xmr and its multicopy MSYq-linked relative Sly, which are upregulated and downregulated, respectively, in the testes of MSYqdel males. Xmr is also expressed during meiotic sex chromosome inactivation (MSCI), indicating a link between the MSCI and the MSYq-dependent gonosomal repression in spermatids. We therefore propose that this repression and MSCI itself are evolutionary adaptations to maintain a normal sex ratio in the face of X/Y antagonism.
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