The Campylobacter jejuni CiaD effector co-opts the host cell protein IQGAP1 to promote cell entry.
Nicholas M NegrettiChristopher R GourleyPrabhat K TalukdarGeremy C ClairCourtney M KlappenbachCody J LauritsenJoshua N AdkinsMichael E KonkelPublished in: Nature communications (2021)
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.
Keyphrases
- single cell
- cell therapy
- dendritic cells
- cell migration
- blood pressure
- binding protein
- cystic fibrosis
- biofilm formation
- signaling pathway
- regulatory t cells
- mesenchymal stem cells
- small molecule
- antimicrobial resistance
- induced apoptosis
- drug delivery
- cancer therapy
- cell proliferation
- living cells
- induced pluripotent stem cells