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PMID:18283110

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Citation

Yang, F, Eckardt, S, Leu, NA, McLaughlin, KJ and Wang, PJ (2008) Mouse TEX15 is essential for DNA double-strand break repair and chromosomal synapsis during male meiosis. J. Cell Biol. 180:673-9

Abstract

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.

Links

PubMed PMC2265566 Online version:10.1083/jcb.200709057

Keywords

Animals; BRCA1 Protein/genetics; BRCA2 Protein/genetics; Carrier Proteins/genetics; Carrier Proteins/metabolism; Cell Cycle Proteins/genetics; Chromosome Pairing/genetics; DNA Breaks, Double-Stranded; DNA Repair/genetics; Endodeoxyribonucleases; Esterases/genetics; Female; Male; Meiosis/genetics; Mice; Mice, Knockout; Mutation; Nuclear Proteins/genetics; Nuclear Proteins/metabolism; Phenotype; Rad51 Recombinase/genetics; Recombination, Genetic/genetics; Sex Characteristics; Spermatids/metabolism; Spermatids/ultrastructure; Spermatogenesis/genetics; Testis/cytology; Testis/growth & development; Testis/metabolism

Significance

Annotations

Gene product Qualifier GO ID GO term name Evidence Code with/from Aspect Notes Status


See also

References

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