Host CDK-1 and formin mediate microvillar effacement induced by enterohemorrhagic Escherichia coli

Enterohemorrhagic Escherichia coli (EHEC) induces changes to the intestinal cell cytoskeleton and formation of attaching and effacing lesions, characterized by the effacement of microvilli and then formation of actin pedestals to which the bacteria are tightly attached. Here, we use a Caenorhabditis elegans model of EHEC infection to show that microvillar effacement is mediated by a signalling pathway including mitotic cyclin-dependent kinase 1 (CDK1) and diaphanous-related formin 1 (CYK1). Similar observations are also made using EHEC-infected human intestinal cells in vitro. Our results support the use of C. elegans as a host model for studying attaching and effacing lesions in vivo, and reveal that the CDK1-formin signal axis is necessary for EHEC-induced microvillar effacement. Enterohemorrhagic Escherichia coli (EHEC) induces formation of attaching and effacing lesions in the intestine. Here, Huang et al. use human intestinal cells and a C. elegans model of infection to show that the process is mediated by a host signaling pathway involving cyclin-dependent kinase CDK1 and formin CYK1.

Automated summary

Enterohemorrhagic Escherichia coli (EHEC) induces attaching and effacing lesions in the intestine through a host signaling pathway involving cyclin-dependent kinase CDK1 and formin CYK1, as demonstrated using human intestinal cells and a C. elegans model of infection.