Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States; California Institute for Quantitative Biosciences, Berkeley, United States; Howard Hughes Medical Institute, Chevy Chase, United States; Biological Systems and Engineering Division, Lawrence Berkeley National Laboratory, Berkeley, United States
Howard Hughes Medical Institute, Chevy Chase, United States; Department of Integrative Biology, University of California, Berkeley, Berkeley, United States
John S Wang
Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States; Howard Hughes Medical Institute, Chevy Chase, United States
Fan Wu
Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States; Howard Hughes Medical Institute, Chevy Chase, United States
Zhouliang Yu
Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States; California Institute for Quantitative Biosciences, Berkeley, United States; Howard Hughes Medical Institute, Chevy Chase, United States; Biological Systems and Engineering Division, Lawrence Berkeley National Laboratory, Berkeley, United States
Chenshu Liu
California Institute for Quantitative Biosciences, Berkeley, United States; Howard Hughes Medical Institute, Chevy Chase, United States
Hyung Jun Kim
Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States
Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States; California Institute for Quantitative Biosciences, Berkeley, United States; Howard Hughes Medical Institute, Chevy Chase, United States; Biological Systems and Engineering Division, Lawrence Berkeley National Laboratory, Berkeley, United States
Meiotic chromosome segregation relies on synapsis and crossover (CO) 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 (DSB) induction. Inactivation of CHK-2 terminates DSB formation and enables CO designation and cell cycle progression. These findings illuminate how meiotic cells ensure CO formation and accurate chromosome segregation.