Polo-like kinase phosphorylation of bilobe-resident TbCentrin2 facilitates flagellar inheritance in Trypanosoma brucei

Author:

de Graffenried Christopher L.1,Anrather Dorothea2,Von Raußendorf Freia3,Warren Graham13

Affiliation:

1. Max F. Perutz Laboratories, Center for Molecular Biology, University of Vienna, 1030 Vienna, Austria

2. Max F. Perutz Laboratories, Department of Biochemistry, Mass Spectrometry Facility, University of Vienna, 1030 Vienna, Austria

3. Max F. Perutz Laboratories, Department of Medical Biochemistry, Medical University of Vienna, 1030 Vienna, Austria

Abstract

In the protist parasite Trypanosoma brucei, the single Polo-like kinase (TbPLK) controls the inheritance of a suite of organelles that help position the parasite's single flagellum. These include the basal bodies, the bilobe, and the flagellar attachment zone (FAZ). TbCentrin2 was previously shown to be a target for TbPLK in vitro, and this is extended in this study to in vivo studies, highlighting a crucial role for serine 54 in the N-terminal domain. Duplication of the bilobe correlates with the presence of TbPLK and phospho-TbCentrin2, identified using phosphospecific antiserum. Mutation of S54 leads to slow growth (S54A) or no growth (S54D), the latter suggesting that dephosphorylation is needed to complete bilobe duplication and subsequent downstream events necessary for flagellum inheritance.

Publisher

American Society for Cell Biology (ASCB)

Subject

Cell Biology,Molecular Biology

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