Genetic Remodeling Transforms E. Coli into Intestinal Pathogen

These effectors subvert host cell processes to promote bacterial colonization.

Investigators at the Hebrew University of Jerusalem showed that the T3SS also functioned to sense the host cell and to trigger in response posttranscriptional remodeling of gene expression in the bacteria. They further showed that upon effector injection, the effector-bound chaperone (CesT), which remained in the EPEC cytoplasm, antagonized the posttranscriptional regulator CsrA.

In obtaining these results, the investigators showed that after attaching to the host by means of pili, the bacteria sensed attachment to the human intestinal cells and activated gene expression in response. This was demonstrated by engineering one of these genes to express a protein that stained the expressing bacteria to appear green under the microscope. Under microscopic examination, the investigators observed that only the attached bacteria fluoresced in bright green, whereas non-attached bacteria remained dark.

"The next steps include mapping in detail the genes that change their expression upon attachment, and describing the precise effects of this expression remodeling,” said senior author Dr. Ilan Rosenshine, professor of bacteriology at the Hebrew University of Jerusalem. “Another important issue is testing whether similar regulation is involved in the infection processes of other pathogens."