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Meiosis relies on the SPO11 endonuclease to generate the recombinogenic DNA double strand breaks (DSBs) required for homologous chromosome synapsis and segregation. The number of meiotic DSBs needs to be sufficient to allow chromosomes to search for and find their homologs, but not excessive to the point of causing genome instability. Here we report that the mammal-specific gene  Tex19 . 1  promotes  Spo11 -dependent recombination in mouse spermatocytes. We show that the chromosome asynapsis previously reported in  Tex19 . 1   -/-   spermatocytes is preceded by reduced numbers of recombination foci in leptotene and zygotene.  Tex19 . 1  is required for normal levels of early  Spo11 -dependent recombination foci during leptotene, but not for upstream events such as MEI4 foci formation or accumulation of H3K4me3 at recombination hotspots. Furthermore, we show that mice carrying mutations in  Ubr2 , which encodes an E3 ubiquitin ligase that interacts with TEX19.1, phenocopy the  Tex19 . 1   -/-   recombination defects. These data suggest that  Tex19 . 1  and  Ubr2  are required for mouse spermatocytes to accumulate sufficient  Spo11 -dependent recombination to ensure that the homology search is consistently successful, and reveal a hitherto unknown genetic pathway promoting meiotic recombination in mammals.

Tex19.1 promotes Spo11-dependent meiotic recombination in mouse spermatocytes