Department of Microbiology and Molecular Genetics, Institute of Medical Research Israel-Canada, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem 9112102, Israel.
Bioinformatics Unit, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem 9112102, Israel.
Science. 2017 Feb 17;355(6326):735-739. doi: 10.1126/science.aah4886.
The mechanisms by which pathogens sense the host and respond by remodeling gene expression are poorly understood. Enteropathogenic (EPEC), the cause of severe intestinal infection, employs a type III secretion system (T3SS) to inject effector proteins into intestinal epithelial cells. These effectors subvert host cell processes to promote bacterial colonization. We show that the T3SS also functions to sense the host cell and to trigger in response posttranscriptional remodeling of gene expression in the bacteria. We further show that upon effector injection, the effector-bound chaperone (CesT), which remains in the EPEC cytoplasm, antagonizes the posttranscriptional regulator CsrA. The CesT-CsrA interaction provokes reprogramming of expression of virulence and metabolic genes. This regulation is likely required for the pathogen's adaptation to life on the epithelium surface.
病原体感知宿主并通过重塑基因表达做出反应的机制尚未完全理解。肠致病性大肠杆菌（EPEC）是严重肠道感染的病原体，它利用 III 型分泌系统（T3SS）将效应蛋白注入肠道上皮细胞。这些效应物颠覆宿主细胞的过程，以促进细菌定植。我们发现 T3SS 还能感知宿主细胞，并在细菌中触发转录后基因表达的重塑反应。我们进一步表明，在效应蛋白注入后，效应蛋白结合的伴侣（CesT），它仍然留在 EPEC 细胞质中，拮抗了转录后调节因子 CsrA。CesT-CsrA 相互作用引发了毒力和代谢基因表达的重新编程。这种调节可能是病原体适应上皮表面生活所必需的。
