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Published online February 18, 2008
doi:10.1083/jcb.200709057
The Journal of Cell Biology, Vol. 180, No. 4, 673-679
The Rockefeller University Press, 0021-9525 $30.00
© 2008 Yang et al.
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 Mouse TEX15 is essential for DNA double-strand break repair and chromosomal synapsis during male meiosis

Fang Yang1, Sigrid Eckardt2, N. Adrian Leu2, K. John McLaughlin2, and Peijing Jeremy Wang1

1 Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104
2 Center for Animal Transgenesis and Germ Cell Research, New Bolton Center, University of Pennsylvania, Kennett Square, PA 19348

Correspondence to Peijing Jeremy Wang: pwang{at}vet.upenn.edu

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.

Abbreviations used in this paper: DSB, double-strand break; ES, embryonic stem; RPA, replication protein A; SC, synaptonemal complex; ssDNA, single-strand DNA.


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