Abstract or Keywords
The coral holobiont is a complex symbiotic association between the polyp animal, photosynthetic dinoflagellates, and their associated microbes. During colonization of coral mucus, opportunistic pathogens, including the white pox pathogen Serratia marcescens PDL100, compete with native bacteria for available nutrients in coral mucus and rely on catabolic enzymes, such as beta -galactosidase and chitinase. This study tested the hypothesis that specific glycosidases and chitinase were critical for the growth of S. marcescens on mucus, and that their inhibition by native coral microbiota reduces fitness of the pathogen. Consistent with this hypothesis, a S. marcescens transposon mutant defective in glycosidase and chitinase activities was unable to compete with the wild type on the mucus of the host coral Acropora palmata. A survey revealed that approximately 8% of culturable coral commensal bacteria have the ability to inhibit glycosidases in the pathogen. In an attempt to understand how coral pathogens infect their hosts, the hypothesis that in the necrotizing coral pathogen S. marcescens PDL100, gacA is involved in the interactions of the pathogen with the polyp hosts was examined. A disruption of the S. marcescens gacA resulted in an increased competitive fitness of the mutant on crude mucus of the host coral Acropora palmata and on the high molecular weight fraction of the mucus, whereas the mutant was as competitive as the wild type on the low molecular weight fraction of the mucus. This indicates a critical role for the gacA-mediated phenotypes in the efficient utilization of coral mucus and establishment within the surface mucopolysaccharide layer. The susceptibility of the sea anemone Aiptasia pallida to common coral pathogens (Serratia marcescens, Vibrio coralliilyticus, and V. shiloi) was also tested. A. pallida responded to the pathogens with symptoms that closely resemble the progression of the coral diseases caused by necrotizing pathogens. Infection studies with this model polyp will elucidate some virulence mechanisms used by coral pathogens to infect and degrade polyps. These results demonstrate, that indeed, coral pathogens rely on specific regulated behaviors to infect their coral hosts and that coral commensal bacteria show the potential to disrupt these early infection strategies.