ArticlePLoS pathogens2018
An orphan kinesin controls trypanosome morphology transitions by targeting FLAM3 to the flagellum.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- FAZ assembly in bloodstream formMolecular biology of the cell · 2023Article
- Diversity in new flagellum tip attachment in bloodstream form African trypanosomes.Molecular microbiology · 2022Article
- Genome-scale RNA interference profiling of Trypanosoma brucei cell cycle progression defects.Nature communications · 2022Article
- Light chain 2 is a Tctex-type related axonemal dynein light chain that regulates directional ciliary motility in Trypanosoma brucei.PLoS pathogens · 2022Article
- Candidates for Balancing Selection in Leishmania donovani Complex Parasites.Genome biology and evolution · 2021Article
- Expansion microscopy facilitates quantitative super-resolution studies of cytoskeletal structures in kinetoplastid parasites.Open biology · 2021Article
- The CRK2-CYC13 complex functions as an S-phase cyclin-dependent kinase to promote DNA replication in Trypanosoma brucei.BMC biology · 2021Article
- APEX2 Proximity Proteomics Resolves Flagellum Subdomains and Identifies Flagellum Tip-Specific Proteins in Trypanosoma brucei.mSphere · 2021Article
- FAZ27 cooperates with FLAM3 and ClpGM6 to maintain cell morphology inJournal of cell science · 2020Article
- Expression and cellular localisation of Trypanosoma cruzi calpains.Memorias do Instituto Oswaldo Cruz · 2020Article
- Calpains of Leishmania braziliensis: genome analysis, differential expression, and functional analysis.Memorias do Instituto Oswaldo Cruz · 2019Article
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2 authors.
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Abstract
Trypanosoma brucei undergoes life cycle form transitions from trypomastigotes to epimastigotes in the insect vector by re-positioning the mitochondrial genome and re-locating the flagellum and flagellum-associated cytoskeletal structures. The mechanism underlying these dramatic morphology transitions remains poorly understood. Here we report the regulatory role of the orphan kinesin KIN-E in controlling trypanosome morphology transitions. KIN-E localizes to the flagellum and is enriched at the flagellar tip, and this localization depends on the C-terminal m-calpain domain III-like domains. Depletion of KIN-E in the trypomastigote form of T. brucei causes major morphology changes and a gradual increase in the level of EP procyclin, generating epimastigote-like cells. Mechanistically, through its C-terminal importin α-like domain, KIN-E targets FLAM3, a flagellar protein involved in morphology transitions, to the flagellum to promote elongation of the flagellum attachment zone and positioning of the flagellum and flagellum-associated cytoskeletal structure, thereby maintaining trypomastigote cell morphology. Our findings suggest that morphology transitions in trypanosomes require KIN-E-mediated transport of FLAM3 to the flagellum.
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