期刊
MOLECULAR CELL
卷 6, 期 5, 页码 989-998出版社
CELL PRESS
DOI: 10.1016/S1097-2765(00)00098-8
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资金
- NCI NIH HHS [P-30 CA08748] Funding Source: Medline
- NHGRI NIH HHS [HG01740] Funding Source: Medline
- NIGMS NIH HHS [GM58673-01] Funding Source: Medline
Spo11, a protein first identified in yeast, is thought to generate the chromosome breaks that initiate meiotic recombination. We now report that disruption of mouse Spoil leads to severe gonadal abnormalities from defective meiosis. Spermatocytes suffer apoptotic death during early prophase; oocytes reach the diplotene/dictyate stage in nearly normal numbers, but most die soon after birth. Consistent with a conserved function in initiating meiotic recombination, Dmc1/Rad51 focus formation is abolished. Spo11 (-/-) meiocytes also display homologous chromosome synapsis defects, similar to fungi but distinct from flies and nematodes. We propose that recombination initiation precedes and is required for normal synapsis in mammals. Our results also support the view that mammalian checkpoint responses to meiotic recombination and/or synapsis defects are sexually dimorphic.
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