Host CDK-1 and formin mediate microvillar effacement induced by enterohemorrhagic Escherichia coli.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 33397943.
- Also identified by DOI 10.1038/s41467-020-20355-1 and PMC identifier 7782584.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
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.
Medical subject headings
- Caenorhabditis elegans Proteins
- Cell Cycle Proteins
- Enterohemorrhagic Escherichia coli
- Host-Pathogen Interactions
- Microvilli