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Human Molecular Genetics Advance Access published online on August 8, 2005
Human Molecular Genetics, doi:10.1093/hmg/ddi304
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© The Author 2005. Published by Oxford University Press. All rights reserved
Received June 24, 2005
Revised July 22, 2005
Accepted August 2, 2005

Article

Deletions on mouse Yq lead to upregulation of multiple X- and Y-linked transcripts in spermatids

Peter J.I. Ellis 1, Emily J. Clemente 1, Penny Ball 2, Aminata Touré 3, Lydia Ferguson 1, James M.A. Turner 3, Kate L. Loveland 2, Nabeel A. Affara 1*, and Paul S. Burgoyne 3

1 Mammalian Molecular Genetics Group, University of Cambridge Department of Pathology, Tennis Court Rd, Cambridge CB2 1QP, UK
2 ARC Centre of Excellence in Biotechnology and Development, Monash Institute for Medical Research, Monash University, Clayton, Melbourne, Vic. 3168, Australia
3 Division 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.
Nabeel A. Affara, E-mail: na{at}mole.bio.cam.ac.uk


  Abstract

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 loss of MSYq-encoded transcripts involve upregulation of multiple X- and Y-linked spermatid-expressed genes, but not related autosomal genes. This therefore indicates that in normal males there is a specific repression of X and Y (gonosomal) transcription in postmeiotic 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 multi-copy gene Xmr and its multi-copy 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 MSCI and the MSYq-dependent gonosomal repression in spermatids. We therefore propose that this repression and/or MSCI itself are evolutionary adaptations to maintain a normal sex ratio in the face of X/Y antagonism.


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