The phytopathogen Dickeya zeae MS2 is a particularly virulent agent of banana soft-rot disease. To begin to understand the banana disease and to understand the role of quorum sensing and quorum sensing-related regulatory elements in D. zeae MS2 we sequenced its genome and queried the sequence for genes coding LuxR homologs. We identified a canonical LuxR-LuxI homolog pair similar to those in other members of the genus Dickeya The quorum-sensing signal for this pair was N-luxR homolog linked to a gene annotated as encoding a proline iminopeptidase. Similar linked pairs have been associated with virulence in other plant pathogens. We show that mutants with deletions in the proline iminopeptidase gene are attenuated for virulence. Surprisingly, a mutant with a deletion in the gene coding the LuxR homolog shows normal virulence.IMPORTANCEDickeya zeae is an emerging banana soft-rot pathogen in China. We used genome sequencing and annotation to create an inventory of potential virulence factors and virulence gene regulators encoded in Dickeya zeae MS2, a particularly virulent strain. We created mutations in several genes and tested these mutants in a banana seedling infection model. A strain with a mutated proline iminopeptidase gene, homologs of which are important for disease in the Xanthomonas spp. phytopathogens, was attenuated for soft-rot symptoms in our model. Understanding how the proline iminopeptidase functions as a virulence factor may lead to insights about how to control the disease and it is of general importance as homologs of the proline iminopeptidase occur in dozens of plant-associated bacteria.