期刊
CELL REPORTS
卷 12, 期 9, 页码 1508-1518出版社
CELL PRESS
DOI: 10.1016/j.celrep.2015.07.063
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资金
- Natural Sciences and Engineering Research Council of Canada
- National Research Council Canada
- Canadian Institutes of Health Research (CIHR)
- Province of Saskatchewan
- Western Economic Diversification Canada
- University of Saskatchewan
- Investigators in Pathogenesis of Infectious Disease Award from the Burroughs Wellcome Fund
- Canadian Foundation for Innovation
- Ontario Innovation Trust
- Ministry of Research and Innovation
- University of Toronto
- CIHR [62890, 93634, GSP-48370]
- Canada Research Chairs program
Intracellular bacterial pathogens of a diverse nature share the ability to evade host immunity by impairing trafficking of endocytic cargo to lysosomes for degradation, a process that is poorly understood. Here, we show that the Salmonella enterica type 3 secreted effector SopD2 mediates this process by binding the host regulatory GTPase Rab7 and inhibiting its nucleotide exchange. Consequently, this limits Rab7 interaction with its dynein- and kinesin-binding effectors RILP and FYCO1 and thereby disrupts host-driven regulation of microtubule motors. Our study identifies a bacterial effector capable of directly binding and thereby modulating Rab7 activity and a mechanism of endocytic trafficking disruption that may provide insight into the pathogenesis of other bacteria. Additionally, we provide a powerful tool for the study of Rab7 function, and a potential therapeutic target.
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