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Published online before print August 23, 2007, 10.1101/gr.6520107
Genome Res. 17:1431-1437, 2007
©2007 by Cold Spring Harbor Laboratory Press; ISSN 1088-9051/07 $5.00
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Letter

Chromosomal rearrangement interferes with meiotic X chromosome inactivation

David Homolka, Robert Ivanek, Jana Capkova, Petr Jansa, and Jiri Forejt1

Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, 142 20 Prague 4, Czech Republic

Heterozygosity for certain mouse and human chromosomal rearrangements is characterized by the incomplete meiotic synapsis of rearranged chromosomes, by their colocalization with the XY body in primary spermatocytes, and by male-limited sterility. Previously, we argued that such X–autosomal associations could interfere with meiotic sex chromosome inactivation. Recently, supporting evidence has reported modifications of histones in rearranged chromosomes by a process called the meiotic silencing of unsynapsed chromatin (MSUC). Here, we report on the transcriptional down-regulation of genes within the unsynapsed region of the rearranged mouse chromosome 17, and on the subsequent disturbance of X chromosome inactivation. The partial transcriptional suppression of genes in the unsynapsed chromatin was most prominent prior to the mid-pachytene stage of primary spermatocytes. Later, during the mid-late pachytene, the rearranged autosomes colocalized with the XY body, and the X chromosome failed to undergo proper transcriptional silencing. Our findings provide direct evidence on the MSUC acting at the mRNA level, and implicate that autosomal asynapsis in meiosis may cause male sterility by interfering with meiotic sex chromosome inactivation.


1 Corresponding author.

E-mail jforejt{at}biomed.cas.cz; fax 420-24106-2154.

[Supplemental material is available online at www.genome.org. The microarray data have been submitted to NCBI/GEO under accession no. GSE7306.]

Article published online before print. Article and publication date are at http://www.genome.org/cgi/doi/10.1101/gr.6520107


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