Author
Listed:
- Cheng-Rung Huang
(National Cheng Kung University
National Cheng Kung University)
- Cheng-Ju Kuo
(National Cheng Kung University
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
National Cheng Kung University)
- Wen-Tsan Chang
(National Cheng Kung University
National Cheng Kung University)
- Yun-Wen Chen
(National Cheng Kung University
National Cheng Kung University)
- Tzer-Min Lee
(Kaohsiung Medical University
National Cheng Kung University)
- Hui-Chen Hsieh
(National Cheng Kung University
National Cheng Kung University)
- Chang-Shi Chen
(National Cheng Kung University
National Cheng Kung University)
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.
Suggested Citation
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 & Chang-Shi Chen, 2021.
"Host CDK-1 and formin mediate microvillar effacement induced by enterohemorrhagic Escherichia coli,"
Nature Communications, Nature, vol. 12(1), pages 1-19, December.
Handle:
RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-020-20355-1
DOI: 10.1038/s41467-020-20355-1
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