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LitR, a newly described transcriptional activator homologue, regulates symbiotic light organ colonization by Vibrio fischeri


, : LitR, a newly described transcriptional activator homologue, regulates symbiotic light organ colonization by Vibrio fischeri. Abstracts of the General Meeting of the American Society for Microbiology 101: 503

The recent discovery of a homologue of the Vibrio cholerae virulence factor, hemagglutinin/protease (hap) in V. fischeri suggested that V. fischeri may also possess a homologue of the hap regulator, hapR. We have characterized a 600 bp ORF in V. fischeri that when translated encodes a peptide, LitR, that shares approximately 60% identity to HapR of V. cholerae and LuxR of V. harveyi. When grown in culture, PMF8, a LitR deficient strain of the bioluminescent squid symbiont V. fischeri ES114, showed no reduction in protease production, but did exhibit a 4-fold reduction in luminescence compared to wild-type. The normal luminescence phenotype was restored by complementation in trans with a wild-type copy of litR. The addition of either aldehyde, a substrate for the luminescence reaction, or autoinducer, which binds to LuxR to activate transcription of luminescence genes, to growing cells of PMF8 also alleviated their luminescence deficiency. Regardless of whether squid were colonized by either V. fischeri ES114 or PMF8, the levels of bacterial luminescence emitted by each colonized squid was essentially equivalent and each strain of V. fischeri reachedroughly the same population density in the squid. However, when squid were exposed to equal numbers of V. fischeri ES114 and PMF8 in a mixed inoculum, cells of PMF8 were competitively dominant, reaching population densities that represented between 69-100% of the total light organ bacterial population. All previous mutations in genes encoding structural or regulatory luminescence functions in symbiotic V. fischeri strains have resulted in either no or severe deficiencies in their ability to colonize squid. In contrast, the litR mutation appears to represent a novel class of mutation in which the loss of a function enhances symbiotic competence. Confirming and characterizing the regulatory activity of litR will provide a way to reveal its symbiotic role in host colonization.

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