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Serratia marcescens  is an opportunistic bacterium that infects a wide range of hosts including humans. It is a potent pathogen in a septic injury model of  Drosophila melanogaster  since a few bacteria directly injected in the body cavity kill the insect within a day. In contrast, flies do not succumb to ingested bacteria for days even though some bacteria cross the intestinal barrier into the hemolymph within hours. The mechanisms by which  S. marcescens  attacks enterocytes and damages the intestinal epithelium remain uncharacterized. To better understand intestinal infections, we performed a genetic screen for loss of virulence of ingested  S. marcescens  and identified FliR, a structural component of the flagellum, as a virulence factor. Next, we compared the virulence of two flagellum mutants  fliR  and  flhD  in two distinct  S. marcescens  strains. Both genes are required for  S. marcescens  to escape the gut lumen into the hemocoel, indicating that the flagellum plays an important role for the passage of bacteria through the intestinal barrier. Unexpectedly,  fliR  but not  flhD  is involved in  S. marcescens -mediated damages of the intestinal epithelium that ultimately contribute to the demise of the host. Our results therefore suggest a flagellum-independent role for  fliR  in bacterial virulence.

The fliR gene contributes to the virulence of S. marcescens in a Drosophila intestinal infection model