Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pbio.3000903
Title: A novel function for CDK2 activity at meiotic crossover sites
Authors: Palmer, N.
Talib, S.Z.A.
Singh, P.
Goh, C.M.F.
Liu, K.
Schimenti, J.C.
Kaldis, P. 
Issue Date: 2020
Publisher: Public Library of Science
Citation: Palmer, N., Talib, S.Z.A., Singh, P., Goh, C.M.F., Liu, K., Schimenti, J.C., Kaldis, P. (2020). A novel function for CDK2 activity at meiotic crossover sites. PLoS Biology 18 (10) : e3000903. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pbio.3000903
Rights: Attribution 4.0 International
Abstract: Genetic diversity in offspring is induced by meiotic recombination, which is initiated between homologs at >200 sites originating from meiotic double-strand breaks (DSBs). Of this initial pool, only 1–2 DSBs per homolog pair will be designated to form meiotic crossovers (COs), where reciprocal genetic exchange occurs between parental chromosomes. Cyclin-dependent kinase 2 (CDK2) is known to localize to so-called “late recombination nodules” (LRNs) marking incipient CO sites. However, the role of CDK2 kinase activity in the process of CO formation remains uncertain. Here, we describe the phenotype of 2 Cdk2 point mutants with elevated or decreased activity, respectively. Elevated CDK2 activity was associated with increased numbers of LRN-associated proteins, including CDK2 itself and the MutL homolog 1 (MLH1) component of the MutL? complex, but did not lead to increased numbers of COs. In contrast, reduced CDK2 activity leads to the complete absence of CO formation during meiotic prophase I. Our data suggest an important role for CDK2 in regulating MLH1 focus numbers and that the activity of this kinase is a key regulatory factor in the formation of meiotic COs. Copyright: © 2020 Palmer et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Source Title: PLoS Biology
URI: https://scholarbank.nus.edu.sg/handle/10635/199689
ISSN: 1544-9173
DOI: 10.1371/journal.pbio.3000903
Rights: Attribution 4.0 International
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