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.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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BRCA1 Protein / genetics
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BRCA2 Protein / genetics
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Carrier Proteins / genetics*
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Carrier Proteins / metabolism
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Cell Cycle Proteins / genetics
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Chromosome Pairing / genetics*
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DNA Breaks, Double-Stranded*
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DNA Repair / genetics*
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DNA-Binding Proteins
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Endodeoxyribonucleases
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Esterases / genetics
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Female
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Male
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Meiosis / genetics*
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Mice
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Mice, Knockout
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Mutation
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Nuclear Proteins / genetics*
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Nuclear Proteins / metabolism
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Phenotype
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Phosphate-Binding Proteins
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Rad51 Recombinase / genetics
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Recombination, Genetic / genetics
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Sex Characteristics
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Spermatids / metabolism*
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Spermatids / ultrastructure
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Spermatogenesis / genetics
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Testis / cytology
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Testis / growth & development
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Testis / metabolism
Substances
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BRCA1 Protein
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BRCA2 Protein
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Carrier Proteins
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Cell Cycle Proteins
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DNA-Binding Proteins
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Dmc1 protein, mouse
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Nuclear Proteins
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Phosphate-Binding Proteins
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Tex15 protein, mouse
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Rad51 Recombinase
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Endodeoxyribonucleases
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Esterases
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meiotic recombination protein SPO11