Abstract
BackgroundPseudoautosomal 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.ResultsWe 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.ConclusionWe propose that the ancestral PAR1 genes share a common epigenetic environment that allows ATRX to control their expression.
Highlights
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
The remaining homology between the sex chromosomes exists in the pseudoautosomal regions (PARs), located at the ends of the X and Y chromosomes [3] and was generated when genetic material from the tips of autosomes translocated to the ancient sex chromosomes [4]
Atrx deletion is achieved by crossing AtrxloxP "floxed" mice to mice that express cyclization recombinase (Cre) under the control of the forebrain-specific forkhead box G1 (Foxg1) promoter [20]
Summary
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. Murine PAR1 homologs have translocated to various autosomes, reflecting the complex recombination history during the evolution of the mammalian X chromosome. Gene dosage between XX females and XY males is usually achieved by the silencing of one X chromosome in every female cell, a process known as X chromosome inactivation (XCI) [5]. Because both males and females have two copies of all PAR genes there is no requirement for dosage compensation and these genes escape this inactivation process [6]. Rodents are strikingly different in that they (page number not for citation purposes)
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