Symbiosis is a major adaptive process allowing bacteria to interact with other organisms to colonise diverse and adverse environments. The genetic mechanisms behind these symbioses are poorly understood despite the fact that some have a major weight on human health and/or welfare. The goal of this project is to investigate the molecular mechanisms involved in monospecific bacterial-host interactions, in particular those occurring between invertebrates and bacteria leading to disease transmission. As a tool, I will use a simple symbiosis model involving Drosophila melanogaster and Pectobacterium carotovorum (formerly Erwinia carotovora), two genetically tractable organisms which will enable the contributions from both the host vector and the bacterial infective agent to be studied. We predict that the genetic determinants of bacterial-host interactions do not differ much and in several cases may rely on a simple genetic basis: the acquisition of a single gene allowing bacteria to colonize the gut of the host. To confirm this hypothesis, we will study the role of EVF (Erwinia virulence factor) in the symbiotic relationship between P. carotovorum and D. melanogaster as well as that of EVF homologues in Photorhabdus luminescens and Xenorhabdus nematophila, both specific nematode symbionts and insect pathogens. In addition, we will dissect the cell-signalling systems, including bacterial quorum sensing, in the insect-borne transmission of P. carotovorum and study the impact of quorum-sensing interference (quorum quenching) in its prevention.