Recruitment of Polo-like kinase couples synapsis to meiotic progression via inactivation of CHK-2

Author:

Zhang Liangyu1234ORCID,Stauffer Weston T35ORCID,Wang John S13,Wu Fan13,Yu Zhouliang1234,Liu Chenshu23,Kim Hyung Jun1,Dernburg Abby F1234ORCID

Affiliation:

1. Department of Molecular and Cell Biology, University of California, Berkeley

2. California Institute for Quantitative Biosciences

3. Howard Hughes Medical Institute

4. Biological Systems and Engineering Division, Lawrence Berkeley National Laboratory

5. Department of Integrative Biology, University of California, Berkeley

Abstract

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.

Funder

Howard Hughes Medical Institute

National Institutes of Health

Publisher

eLife Sciences Publications, Ltd

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine,General Neuroscience

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