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Publication : Mouse TEX15 is essential for DNA double-strand break repair and chromosomal synapsis during male meiosis.

First Author  Yang F Year  2008
Journal  J Cell Biol Volume  180
Issue  4 Pages  673-9
PubMed ID  18283110 Mgi Jnum  J:135578
Mgi Id  MGI:3794139 Doi  10.1083/jcb.200709057
Citation  Yang F, et al. (2008) Mouse TEX15 is essential for DNA double-strand break repair and chromosomal synapsis during male meiosis. J Cell Biol 180(4):673-9
abstractText  During meiosis, homologous chromosomes undergo synapsis and recombination. We identify TEX15 as a novel protein that is required for chromosomal synapsis and meiotic recombination. Loss of TEX15 function in mice causes early meiotic arrest in males but not in females. Specifically, TEX15-deficient spermatocytes exhibit a failure in chromosomal synapsis. In mutant spermatocytes, DNA double-strand breaks (DSBs) are formed, but localization of the recombination proteins RAD51 and DMC1 to meiotic chromosomes is severely impaired. Based on these data, we propose that TEX15 regulates the loading of DNA repair proteins onto sites of DSBs and, thus, its absence causes a failure in meiotic recombination.
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