Current Biology
Volume 16, Issue 24, 19 December 2006, Pages 2473-2479
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Two Distinct Surveillance Mechanisms Monitor Meiotic Chromosome Metabolism in Budding Yeast

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Summary

Meiotic recombination is initiated by Spo11-generated DNA double-strand breaks (DSBs) [1]. A fraction of total DSBs is processed into crossovers (CRs) between homologous chromosomes, which promote their accurate segregation at meiosis I (MI) [2]. The coordination of recombination-associated events and MI progression is governed by the “pachytene checkpoint” [3], which in budding yeast requires Rad17, a component of a PCNA clamp-like complex, and Pch2, a putative AAA-ATPase 3, 4, 5, 6, 7. We show that two genetically separable pathways monitor the presence of distinct meiotic recombination-associated lesions: First, delayed MI progression in the presence of DNA repair intermediates is suppressed when RAD17 or SAE2, encoding a DSB-end processing factor 8, 9, is deleted. Second, delayed MI progression in the presence of aberrant synaptonemal complex (SC) is suppressed when PCH2 is deleted. Importantly, ZIP1, encoding the central element of the SC [10], is required for PCH2-dependent checkpoint activation. Analysis of the rad17Δ pch2Δ double mutant revealed a redundant function regulating interhomolog CR formation. These findings suggest a link between the surveillance of distinct recombination-associated lesions, control of CR formation kinetics, and regulation of MI timing. A PCH2-ZIP1-dependent checkpoint in meiosis is likely conserved among synaptic organisms from yeast to human 6, 11.

DNA

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