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.

中文翻译：

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肠致病性大肠杆菌感染过程中III型效应子的表达，分泌和易位动力学。

肠致病性大肠杆菌（EPEC）是全世界婴儿腹泻和死亡的重要原因。EPEC基因组中肠上皮细胞侵染（LEE）致病岛的所在地编码3型分泌系统（T3SS）。这种纳米机器直接将复杂的效应子库注射到宿主细胞中，这对于EPEC发病机理至关重要。为了定居肠道粘膜，EPEC响应宿主环境信号改变其基因表达。LEE的调控已被广泛研究，揭示了转录调控的关键机制，最近在转录后和翻译后的水平上也有揭示。此外，T3SS的组装和分泌是高度协调的过程，可确保细胞接触后效应子的分层传递。EPEC效应子和毒力因子不仅操纵宿主细胞过程，而且还通过控制T3SS的形成来调节效应子的转运。在这篇综述中，我们着重于对EPEC毒力基因的调节以及对效应物分泌和转运的调节。