Mouse TEX15 is essential for DNA double-strand break repair and chromosomal synapsis during male meiosis
نویسندگان
چکیده
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.
منابع مشابه
P-230: Analysis of TEX15 Expression in Testis Tissues of Severe Oligozoospermic and Non-Obstructive Azoospermic Men Referred to Royan Institute
Background: TEX15 is a novel protein that is required for chromosomal synapsis and meiotic recombination. Human TEX15 is located on chromosome 8(8p12 region) and expressed in testis and ovary, as is its mouse ortholog. 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 ...
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