The kinetoplastid-specific phosphatase KPP1 attenuates PLK activity to facilitate flagellum inheritance in Trypanosoma brucei.

ABSTRACT: Trypanosoma brucei, an important human parasite, has a flagellum that controls cell motility, morphogenesis, proliferation, and cell-cell communication. Inheritance of the newly assembled flagellum during the cell cycle requires the Polo-like kinase homolog TbPLK and the kinetoplastid-specific protein phosphatase KPP1, although whether TbPLK acts on KPP1 or vice versa has been unclear. Here, we showed that dephosphorylation of TbPLK on Thr¹²⁵ by KPP1 maintained low TbPLK activity in the flagellum-associated hook complex structure, thereby ensuring proper flagellum positioning and attachment. This dephosphorylation event required the recognition of phosphorylated Thr¹⁹⁸ in the activation loop of TbPLK by the N-terminal Plus3 domain of KPP1 and the dephosphorylat

SUBMITTER: An T 

PROVIDER: S-EPMC7985912 | biostudies-literature | 2021 Feb

REPOSITORIES: biostudies-literature