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SKIP, the Host Target of the Salmonella Virulence Factor SifA, Promotes Kinesin-1-Dependent Vacuolar Membrane Exchanges.

Abstract : In Salmonella-infected cells, the bacterial effector SifA forms a functional complex with the eukaryotic protein SKIP (SifA and kinesin-interacting protein). The lack of either partner has important consequences on the intracellular fate and on the virulence of this pathogen. In addition to SifA, SKIP binds the microtubule-based motor kinesin-1. Yet the absence of SifA or SKIP results in an unusual accumulation of kinesin-1 on the bacterial vacuolar membrane. To understand this apparent contradiction, we investigated the interaction between SKIP and kinesin-1 and the function of this complex. We show that the C-terminal RUN (RPIP8, UNC-14 and NESCA) domain of SKIP interacted specifically with the tetratricopeptide repeat (TPR) domain of the kinesin light chain. Overexpression of SKIP induced a microtubule- and kinesin-1-dependent anterograde movement of late endosomal/lysosomal compartments. In infected cells, SifA contributed to the fission of vesicles from the bacterial vacuole and the SifA/SKIP complex was required for the formation and/or the anterograde transport of kinesin-1-enriched vesicles. These observations reflect the role of SKIP as a linker and/or an activator for kinesin-1.
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https://hal.archives-ouvertes.fr/hal-00503009
Contributor : Marie Laure Haon Connect in order to contact the contributor
Submitted on : Friday, July 16, 2010 - 12:30:46 PM
Last modification on : Sunday, June 26, 2022 - 11:52:00 AM

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Audrey Dumont, Emmanuel Boucrot, Stéphanie Drevensek, Vanessa Daire, Jean-Pierre Gorvel, et al.. SKIP, the Host Target of the Salmonella Virulence Factor SifA, Promotes Kinesin-1-Dependent Vacuolar Membrane Exchanges.. Traffic, Wiley, 2010, 11 (7), pp.899-911. ⟨10.1111/j.1600-0854.2010.01069.x⟩. ⟨hal-00503009⟩

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