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Open Access Research article

The SWI/SNF protein ATRX co-regulates pseudoautosomal genes that have translocated to autosomes in the mouse genome

Michael A Levy14, Andrew D Fernandes12, Deanna C Tremblay14, Claudia Seah34 and Nathalie G Bérubé134*

Author Affiliations

1 Department of Biochemistry, University of Western Ontario, London, N6A 4L6, Canada

2 Applied Mathematics, University of Western Ontario, London, N6A 4L6, Canada

3 Paediatrics, University of Western Ontario, London, N6A 4L6, Canada

4 Children's Health Research Institute, Lawson Health Research Institute, 800 Commissioners Road East, London, N6C 2V5, Canada

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BMC Genomics 2008, 9:468  doi:10.1186/1471-2164-9-468

Published: 8 October 2008

Abstract

Background

Pseudoautosomal regions (PAR1 and PAR2) in eutherians retain homologous regions between the X and Y chromosomes that play a critical role in the obligatory X-Y crossover during male meiosis. Genes that reside in the PAR1 are exceptional in that they are rich in repetitive sequences and undergo a very high rate of recombination. Remarkably, murine PAR1 homologs have translocated to various autosomes, reflecting the complex recombination history during the evolution of the mammalian X chromosome.

Results

We now report that the SNF2-type chromatin remodeling protein ATRX controls the expression of eutherian ancestral PAR1 genes that have translocated to autosomes in the mouse. In addition, we have identified two potentially novel mouse PAR1 orthologs.

Conclusion

We propose that the ancestral PAR1 genes share a common epigenetic environment that allows ATRX to control their expression.