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. 2000 Nov;6(5):989-98.
doi: 10.1016/s1097-2765(00)00098-8.

Chromosome synapsis defects and sexually dimorphic meiotic progression in mice lacking Spo11

F Baudat  1 , K Manova, J P Yuen, M Jasin, S Keeney
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Free article

Chromosome synapsis defects and sexually dimorphic meiotic progression in mice lacking Spo11

F Baudat et al. Mol Cell. 2000 Nov.
Free article

Abstract

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 Spo11 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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