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

Cheng-Rung Huang, Cheng-Ju Kuo, Chih-Wen Huang, Yu-Ting Chen, Bang-Yu Liu, Chung-Ta Lee, Po-Lin Chen, Wen-Tsan Chang, Yun-Wen Chen, Tzer-Min Lee, Hui-Chen Hsieh and Chang-Shi Chen ()
Additional contact information
Cheng-Rung Huang: National Cheng Kung University
Cheng-Ju Kuo: National Cheng Kung University
Chih-Wen Huang: National Cheng Kung University
Yu-Ting Chen: National Cheng Kung University
Bang-Yu Liu: National Cheng Kung University
Chung-Ta Lee: National Cheng Kung University
Po-Lin Chen: National Cheng Kung University
Wen-Tsan Chang: National Cheng Kung University
Yun-Wen Chen: National Cheng Kung University
Tzer-Min Lee: Kaohsiung Medical University
Hui-Chen Hsieh: National Cheng Kung University
Chang-Shi Chen: National Cheng Kung University

Nature Communications, 2021, vol. 12, issue 1, 1-19

Abstract: 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.

Date: 2021
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DOI: 10.1038/s41467-020-20355-1

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