Polo-like kinase phosphorylation of the orphan kinesin KIN-G negatively regulates centrin arm biogenesis in Trypanosoma brucei.
- Open access
Polo-like kinase phosphorylation of KIN-G inhibits centrin arm formation in Trypanosoma brucei, affecting cell division and flagellum positioning.
- Why it matters: Understanding how cytoskeletal structures are regulated is crucial for insights into parasite cell division and motility, which are potential targets for intervention.
- What they did: The study used in vitro phosphorylation assays and mutant expression in T. brucei to show TbPLK phosphorylates KIN-G at Thr301, disrupting its microtubule-binding activity and impairing centrin arm biogenesis.
- The result: Phosphorylation of KIN-G by TbPLK negatively regulates its function, revealing a cycle of phosphorylation/dephosphorylation that controls key cytoskeletal structures and cell division processes in T. brucei.