Litcius/Paper detail

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

Cheng-Rung Huang, Cheng‐Ju Kuo, Chih-Wen Huang, Yuting 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

2021Nature Communications21 citationsDOIOpen Access PDF

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.

Topics & Concepts

BiologyCell biologyCaenorhabditis elegansEscherichia coliForminsCyclin-dependent kinase 1ActinMicrobiologyActin cytoskeletonCytoskeletonCellGeneticsCell cycleGeneGut microbiota and healthEscherichia coli research studiesGenetics, Aging, and Longevity in Model Organisms
Host CDK-1 and formin mediate microvillar effacement induced by enterohemorrhagic Escherichia coli | Litcius