التفاصيل البيبلوغرافية
| العنوان: |
An orphan kinesin controls trypanosome morphology transitions by targeting FLAM3 to the flagellum. |
| المؤلفون: |
An, Tai, Li, Ziyin |
| المصدر: |
PLoS Pathogens; 5/29/2018, Vol. 14 Issue 5, p1-24, 24p |
| مصطلحات موضوعية: |
FLAGELLA (Microbiology), TRYPANOSOMA brucei, KINESIN, CYTOSKELETON, CELL morphology |
| مستخلص: |
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. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
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