The Campylobacter jejuni CiaD effector co-opts the host cell protein IQGAP1 to promote cell entry

Nicholas M. Negretti, Christopher R. Gourley, Prabhat K. Talukdar, Geremy Clair, Courtney M. Klappenbach, Cody J. Lauritsen, Joshua N. Adkins and Michael E. Konkel ()
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Nicholas M. Negretti: College of Veterinary Medicine, Washington State University
Christopher R. Gourley: College of Veterinary Medicine, Washington State University
Prabhat K. Talukdar: College of Veterinary Medicine, Washington State University
Geremy Clair: Integrative Omics, Pacific Northwest National Laboratory
Courtney M. Klappenbach: College of Veterinary Medicine, Washington State University
Cody J. Lauritsen: College of Veterinary Medicine, Washington State University
Joshua N. Adkins: Integrative Omics, Pacific Northwest National Laboratory
Michael E. Konkel: College of Veterinary Medicine, Washington State University

Nature Communications, 2021, vol. 12, issue 1, 1-14

Abstract: Abstract Campylobacter jejuni is a foodborne pathogen that binds to and invades the epithelial cells lining the human intestinal tract. Maximal invasion of host cells by C. jejuni requires cell binding as well as delivery of the Cia proteins (Campylobacter invasion antigens) to the host cell cytosol via the flagellum. Here, we show that CiaD binds to the host cell protein IQGAP1 (a Ras GTPase-activating-like protein), thus displacing RacGAP1 from the IQGAP1 complex. This, in turn, leads to the unconstrained activity of the small GTPase Rac1, which is known to have roles in actin reorganization and internalization of C. jejuni. Our results represent the identification of a host cell protein targeted by a flagellar secreted effector protein and demonstrate that C. jejuni-stimulated Rac signaling is dependent on IQGAP1.

Date: 2021
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DOI: 10.1038/s41467-021-21579-5

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