Erwinia carotovora Quorum Sensing System Regulates Host-Specific Virulence Factors and Development Delay in Drosophila melanogaster.

Multihost bacteria have to rapidly adapt to drastic environmental changes, relying on a fine integration of multiple stimuli for an optimal genetic response. spp. are phytopathogens that cause soft-rot disease. Strain in particular is a model for bacterial oral-route infection in as it harbors a unique gene, , that encodes the virulence factor (Evf), which is a major determinant for infection of the gut. However, the factors involved in the regulation of expression are poorly understood. We investigated whether could be controlled by quorum sensing as, in the genus, quorum sensing regulates pectolytic enzymes, the major virulence factors needed to infect plants. Here, we show that transcription of is positively regulated by quorum sensing in via acyl-homoserine lactone (AHL) signal synthase ExpI and AHL receptors ExpR1 and ExpR2. We also show that the load of in the gut depends upon the quorum sensing-mediated regulation of Furthermore, we demonstrate that larvae infected with suffer a developmental delay as a direct consequence of the regulation of via quorum sensing. Finally, we demonstrate that is coexpressed with plant cell wall-degrading enzymes (PCWDE) during plant infection in a quorum sensing-dependent manner. Overall, our results show that relies on quorum sensing to control production of both pectolytic enzymes and Evf. This regulation influences the interaction of with its two known hosts, indicating that quorum sensing signaling may impact bacterial dissemination via insect vectors that feed on rotting plants. Integration of genetic networks allows bacteria to rapidly adapt to changing environments. This is particularly important in bacteria that interact with multiple hosts. is a plant pathogen that uses as a vector. To interact with these two hosts, uses different sets of virulence factors: plant cell wall-degrading enzymes to infect plants and the virulence factor () to infect Our work shows that, despite the virulence factors being specific for each host, both sets are coactivated by homoserine lactone quorum sensing and by the two-component GacS/A system in infected plants. This regulation is essential for loads in the gut of and minimizes the developmental delay caused by the bacteria with respect to the insect vector. Our findings provide evidence that coactivation of the host-specific factors in the plant may function as a predictive mechanism to maximize the probability of transit of the bacteria between hosts.