Dynamics of expression, secretion and translocation of type III effectors during enteropathogenic Escherichia coli infection.

Enteropathogenic Escherichia coli (EPEC) is an important cause of infant diarrhea and mortality worldwide. The locus of enterocyte effacement (LEE) pathogenicity island in the EPEC genome encodes a type 3 secretion system (T3SS). This nanomachine directly injects a sophisticated arsenal of effectors into host cells, which is critical for EPEC pathogenesis. To colonize the gut mucosa, EPEC alters its gene expression in response to host environmental signals. Regulation of the LEE has been studied extensively, revealing key mechanisms of transcriptional regulation, and more recently at the posttranscriptional and posttranslational levels. Moreover, the T3SS assembly and secretion is a highly coordinated process that ensures hierarchical delivery of effectors upon cell contact. EPEC effectors and virulence factors not only manipulate host cellular processes, but also modulate effector translocation by controlling T3SS formation. In this review, we focus on the regulation of EPEC virulence genes and modulation of effector secretion and translocation.