The induction of luminescence in Vibrio harveyi is dependent on the production of autoinducers which partake in a complex system of signal transduction through a central regulator LuxO. SAM is one of the key metabolites required in biological systems and plays a central role in the formation of the two autoinducers (AI-1 and AI-2) in the quorum sensing systems controlling luminescence in Vibrio harveyi. AI-1, N-hydroxybutanylhomoserine lactone is believed to arise from the reaction of SAM and N-hydroxybutanoyl-ACP catalyzed by LuxM. Strong evidence exists that AI-2 arises from cleavage of SAM to S-adenoysl homocysteine and then to S-ribosylhomocysteine which is then converted by LuxS into a ribosyl derivative that cyclizes into a furanone. We therefore predicted that genes that limit the level of SAM should inhibit luminescence while genes that stimulate its synthesis should decrease luminescence. Recently we have found that proteins involved in the regulation and metabolism of SAM greatly affect the level of luminescence in autoinducer-deficient mutants of V. harveyi. As these proteins can be related to the synthesis and degradation of SAM and/or methionine (Met), elucidation of the mechanism by which these proteins affect luminescence including potential effects on the levels of autoinducers and other regulatory elements involved in the quorum sensing system is of primary interest. These studies should prove valuable in identifying the control and specific pathways responsible for the synthesis of the autoinducers.
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