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Department of Animal Sciences
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The Hebrew University of Jerusalem.

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Host cell attachment elicits posttranscriptional regulation in infecting enteropathogenic bacteria

Citation:

Katsowich, N. ; Elbaz, N. ; Pal, R. R. ; Mills, E. ; Kobi, S. ; Kahan, T. ; Rosenshine, I. Host cell attachment elicits posttranscriptional regulation in infecting enteropathogenic bacteria. Science 2017, 355, 735–739.

Abstract:

Escherichia coli is transformed from a commensal organism into a pathogen by acquisition of genetic elements called pathogenicity islands (PAIs). Katsowich et al. investigated how the PAI virulence genes of enteropathogenic E. coli (EPEC) respond when the bacterium attaches to a host gut cell. EPEC first sticks to the host by means of pili and then uses a PAI-encoded type 3 secretion system (T3SS) to inject multiple effectors into the host cell. But not all virulence mediators are injected. For example, CesT, a bacterial chaperone, delivers virulence effectors into the T3SS apparatus. Then, within the bacterial cytoplasm, it interacts with a gene repressor called CsrA, which reprograms bacterial gene expression to help the bacteria to adapt to epithelial cell–associated life.Science, this issue p. 735The mechanisms by which pathogens sense the host and respond by remodeling gene expression are poorly understood. Enteropathogenic Escherichia coli (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.

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