Host CDK-1 and formin mediate microvillar effacement induced by enterohemorrhagic Escherichia coli.
Cheng-Rung HuangCheng-Ju KuoChih-Wen HuangYu-Ting ChenBang-Yu LiuChung-Ta LeePo Lin ChenWen-Tsan ChangYun-Wen ChenTzer-Min LeeHui-Chen HsiehChang-Shi ChenPublished in: Nature communications (2021)
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.
Keyphrases
- cell cycle
- escherichia coli
- cell proliferation
- endothelial cells
- single cell
- induced apoptosis
- high glucose
- klebsiella pneumoniae
- genome wide
- stem cells
- biofilm formation
- drug induced
- cell therapy
- staphylococcus aureus
- signaling pathway
- endoplasmic reticulum stress
- tyrosine kinase
- pseudomonas aeruginosa
- cell death
- multidrug resistant