Clathrin‐associated Endocytic Proteins Eps15 and Epsin are Crucial for the Formation of Enteropathogenic E. coli (EPEC) pedestals

Abstract

Enteropathogenic E.coli (EPEC) are primarily extracellular pathogens that cause severe infantile diarrhea. The hallmark of EPEC pathogenesis is the generation of actin‐rich structures known as pedestals. Surprising evidence has revealed that while they persistently reside at an extracellular space, EPEC require the receptor‐mediated endocytosis protein, clathrin, for pedestal formation. In order to understand the strategies EPEC utilize to usurp endocytosis, we examined the roles of three major endocytic components: AP‐2, Eps15 and epsin, during pedestals formation. We found that pedestal formations required the recruitment of Eps15 and epsin, but not AP‐2. AP‐2 is known to provide linkage between Eps15, epsin and clathrin during the clathrin‐coated pit assembly process to complete endocytosis. Together, these results reveal a novel endocytic protein manipulation strategy employed by EPEC, supporting the recent paradigm that endocytic proteins are important for EPEC‐mediated disease.Grant Funding Source: CIHR