Phage-encoded sRNA counteracts xenogeneic silencing in pathogenic E. coli

Transcriptomic profiling further revealed that HnrS activates genes involved in nitrate/nitrite respiration and nitric oxide resistance, metabolic pathways the contribute to survival in the inflamed gastrointestinal tract. Deletion of hnrS reduced expression of nitrate reductase genes and impaired actin pedestal formation on host epithelial cells. Our results indicate that multiple hnrS copies encoded on prophages provide a counter-silencing mechanism that reduces Hha–H-NS repression at specific virulence loci.

This likely enables expression of horizontally acquired genes without broadly disrupting the global H-NS regulon. HnrS illustrates how mobile genetic elements can deploy sRNAs to counteract xenogeneic silencing and promote virulence gene expression, enhancing colonisation of the host.