Meiotic cell cycle progression requires adaptation to a constitutive DNA damage signal

Abstract

Meiotic chromosome segregation relies on synapsis and crossover recombination between homologous chromosomes. These processes require multiple steps that are coordinated by the meiotic cell cycle and monitored by surveillance mechanisms. In diverse species, failures in chromosome synapsis can trigger a cell cycle delay and/or lead to apoptosis. How this key step in "homolog engagement" is sensed and transduced by meiotic cells is unknown. Here we report that in C. elegans, recruitment of the Polo-like kinase PLK-2 to the synaptonemal complex triggers phosphorylation and inactivation of CHK-2, an early meiotic kinase required for pairing, synapsis, and double-strand break induction. Inactivation of CHK-2 ends double-strand break formation and promotes crossover designation and cell cycle progression. These findings illuminate how meiotic cells ensure crossover formation and accurate chromosome segregation. SummaryAccurate chromosome segregation during meiosis requires crossovers between each pair of homologs. Zhang et al. show that meiotic progression in C. elegans involves inactivation of CHK-2 by PLK-2 in response to synapsis and formation of crossover precursors on all chromosomes.