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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...

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Detalles Bibliográficos
Autores principales: Huang, Cheng-Rung, Kuo, Cheng-Ju, Huang, Chih-Wen, Chen, Yu-Ting, Liu, Bang-Yu, Lee, Chung-Ta, Chen, Po-Lin, Chang, Wen-Tsan, Chen, Yun-Wen, Lee, Tzer-Min, Hsieh, Hui-Chen, Chen, Chang-Shi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7782584/
https://www.ncbi.nlm.nih.gov/pubmed/33397943
http://dx.doi.org/10.1038/s41467-020-20355-1
Descripción
Sumario: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.