Jan 2, 2016

Loss of the BBSome perturbs endocytic trafficking and disrupts virulence of Trypanosoma brucei

Proceedings of the National Academy of Sciences of the United States of America
Gerasimos LangousisKent L Hill

Abstract

Cilia (eukaryotic flagella) are present in diverse eukaryotic lineages and have essential motility and sensory functions. The cilium's capacity to sense and transduce extracellular signals depends on dynamic trafficking of ciliary membrane proteins. This trafficking is often mediated by the Bardet-Biedl Syndrome complex (BBSome), a protein complex for which the precise subcellular distribution and mechanisms of action are unclear. In humans, BBSome defects perturb ciliary membrane protein distribution and manifest clinically as Bardet-Biedl Syndrome. Cilia are also important in several parasites that cause tremendous human suffering worldwide, yet biology of the parasite BBSome remains largely unexplored. We examined BBSome functions in Trypanosoma brucei, a flagellated protozoan parasite that causes African sleeping sickness in humans. We report that T. brucei BBS proteins assemble into a BBSome that interacts with clathrin and is localized to membranes of the flagellar pocket and adjacent cytoplasmic vesicles. Using BBS gene knockouts and a mouse infection model, we show the T. brucei BBSome is dispensable for flagellar assembly, motility, bulk endocytosis, and cell viability but required for parasite virulence. Quantitative ...Continue Reading

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Mentioned in this Paper

Ubiquitin-dependent Protein Catabolic Process
Establishment and Maintenance of Localization
Mastigophora
Tissue Membrane
Endocytosis
Extracellular
Membrane
Cell Motility
Cytoplasmic Vesicles
Pathogenic Organism

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