The MAST kinase KIN-4 provides the Greatwall activity in C. elegans

ABSTRACT: Mitotic entry is triggered by the Cyclin B-Cdk1 kinase, which phosphorylates numer-ous substrates. The accumulation of these phosphorylated substrates relies on inhib-iting the opposing PP2A-B55 phosphatase. With its asynchronous cell divisions, the C. elegans embryo is an attractive model for dissecting how the cross-talk between Cyclin B-Cdk1 and PP2A-B55 ensures cell cycle length during development. Howev-er, the mechanisms that control PP2A-B55 activity have remained elusive in C. elegans because its genome encodes no obvious homolog of the Greatwall kinase, which inhibits PP2A-B55 in other metazoans. Here, we show that the single MAST kinase KIN-4, previously associated with aging and thermotaxis phenotypes, provides the Greatwall activity in C. elegans and can functionally replace Greatwall in the het-erologous Xenopus system. Furthermore, we show that a balance between Cyclin B-Cdk1 and PP2A-B55 activity, regulated by KIN-4, is essential to ensure asynchronous cell divisions. Our findings resolve a long-standing puzzle related to the supposed absence of a Greatwall-like pathway in C. elegans and highlight a novel aspect of PP2A-B55 regulation by MAST kinases with implications in several biological pro-cesses

INSTRUMENT(S):

ORGANISM(S): Caenorhabditis Elegans

SUBMITTER: Guillaume CHEVREUX  

LAB HEAD: Lionel Pintard

PROVIDER: PXD054396 | Pride | 2025-05-07

REPOSITORIES: Pride