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dc.contributor.authorJavary, Joaquim
dc.contributor.authorGoupil, Eugénie
dc.contributor.authorSoulez, Mathilde
dc.contributor.authorKanshin, Evgeny
dc.contributor.authorBouchard, Antoine
dc.contributor.authorSeternes, Ole Morten
dc.contributor.authorThibault, Pierre
dc.contributor.authorLabbé, Jean-Claude
dc.contributor.authorMeloche, Sylvain
dc.description.abstractExtracellular signal-regulated kinase 3 (ERK3) is a poorly characterized member of the mitogen-activated protein (MAP) kinase family. Functional analysis of the ERK3 signaling pathway has been hampered by a lack of knowledge about the substrates and downstream effectors of the kinase. Here, we used large-scale quantitative phosphoproteomics and targeted gene silencing to identify direct ERK3 substrates and gain insight into its cellular functions. Detailed validation of one candidate substrate identified the gelsolin/villin family member supervillin (SVIL) as a <i>bona fide</i> ERK3 substrate. We show that ERK3 phosphorylates SVIL on Ser245 to regulate myosin II activation and cytokinesis completion in dividing cells. Depletion of SVIL or ERK3 leads to increased cytokinesis failure and multinucleation, a phenotype rescued by wild type SVIL but not by the non-phosphorylatable S245A mutant. Our results unveil a new function of the atypical MAP kinase ERK3 in cell division and the regulation of cell ploidy.en_US
dc.identifier.citationJavary, Goupil, Soulez, Kanshin, Bouchard, Seternes, Thibault, Labbé, Meloche. Phosphoproteomic analysis identifies supervillin as an ERK3 substrate regulating cytokinesis and cell ploidy. Journal of Cellular Physiology. 2022en_US
dc.identifier.cristinIDFRIDAID 2107410
dc.relation.journalJournal of Cellular Physiology
dc.rights.holderCopyright 2022 The Author(s)en_US
dc.rightsAttribution 4.0 International (CC BY 4.0)en_US
dc.titlePhosphoproteomic analysis identifies supervillin as an ERK3 substrate regulating cytokinesis and cell ploidyen_US
dc.typeJournal articleen_US
dc.typePeer revieweden_US

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Attribution 4.0 International (CC BY 4.0)
Except where otherwise noted, this item's license is described as Attribution 4.0 International (CC BY 4.0)