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Article: A novel function for CDK2 activity at meiotic crossover sites

TitleA novel function for CDK2 activity at meiotic crossover sites
Authors
Editors
Editor(s):Zanders, S
Issue Date2020
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosbiology.org/plosonline/?request=index-html
Citation
PLoS Biology, 2020, v. 18 n. 10, p. article no. e3000903 How to Cite?
AbstractGenetic 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 MutLγ 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.
Persistent Identifierhttp://hdl.handle.net/10722/304574
ISSN
2023 Impact Factor: 7.8
2023 SCImago Journal Rankings: 3.822
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorPalmer, N-
dc.contributor.authorTalib, SZA-
dc.contributor.authorSingh, P-
dc.contributor.authorGoh, CMF-
dc.contributor.authorLiu, K-
dc.contributor.authorSchimenti, JC-
dc.contributor.authorKaldis, P-
dc.contributor.editorZanders, S-
dc.date.accessioned2021-09-23T09:02:01Z-
dc.date.available2021-09-23T09:02:01Z-
dc.date.issued2020-
dc.identifier.citationPLoS Biology, 2020, v. 18 n. 10, p. article no. e3000903-
dc.identifier.issn1544-9173-
dc.identifier.urihttp://hdl.handle.net/10722/304574-
dc.description.abstractGenetic 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 MutLγ 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.-
dc.languageeng-
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosbiology.org/plosonline/?request=index-html-
dc.relation.ispartofPLoS Biology-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleA novel function for CDK2 activity at meiotic crossover sites-
dc.typeArticle-
dc.identifier.emailLiu, K: kliugc@hku.hk-
dc.identifier.authorityLiu, K=rp02475-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pbio.3000903-
dc.identifier.pmid33075054-
dc.identifier.pmcidPMC7595640-
dc.identifier.scopuseid_2-s2.0-85094571971-
dc.identifier.hkuros325146-
dc.identifier.volume18-
dc.identifier.issue10-
dc.identifier.spagearticle no. e3000903-
dc.identifier.epagearticle no. e3000903-
dc.identifier.isiWOS:000584564600001-
dc.publisher.placeUnited States-

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