Authors
Yasuhiro Kurasawa, Qing Zhou, Kyu Joon Lee, Huiqing Hu, Ziyin Li
Published in
eLife. Volume 15. Sep 04, 2026. Epub Sep 04, 2026.
Abstract
The unicellular parasite Trypanosoma brucei assembles a motile flagellum that is required for locomotion, cell division plane placement, and cell-cell communication. Inheritance of the flagellum during the cell cycle relies on the faithful duplication/segregation of multiple flagellum-associated cytoskeletal structures, including a centrin-marked, bar-shaped structure termed centrin arm, which also determines the site for Golgi assembly. Biogenesis of the centrin arm requires the Polo-like kinase homolog TbPLK and the orphan kinesin KIN-G, but the mechanistic role of TbPLK in centrin arm biogenesis remains elusive. Here, we report that TbPLK phosphorylates KIN-G, disrupts its microtubule-binding activity, and negatively regulates its function. TbPLK phosphorylates KIN-G in vitro at multiple residues, two of which are in vivo TbPLK phosphosites, including the Thr301 residue within one of the microtubule-binding motifs of the kinesin motor domain. Phosphorylation of Thr301 by TbPLK inhibits the microtubule-binding activity of KIN-G in vitro, and expression of a Thr301 phospho-mimic mutant in T. brucei disrupts centrin arm integrity, Golgi duplication, flagellum attachment zone elongation, flagellum positioning, and cell division plane placement. In wild-type T. brucei cells, Thr301 phosphorylation occurs on a small portion of the KIN-G population, suggesting that KIN-G undergoes phosphorylation/dephosphorylation cycles to regulate its activity. Together, these findings uncover a negative role of TbPLK-mediated phosphorylation of KIN-G in regulating centrin arm biogenesis in trypanosomes.
PMID:
42696466
Bibliographic data and abstract were imported from PubMed on 05 Sep 2026.
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