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首页> 外文会议>12th Symposium on Bioluminescence and Chemiluminescence, Apr 5-9, 2002, Robinson College, University of Cambridge, UK >EFFECT OF SAM-RELATED STRUCTURAL AND REGULATORY PROTEINS ON LUMINESCENCE IN VIBRIO HAR VEYI
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EFFECT OF SAM-RELATED STRUCTURAL AND REGULATORY PROTEINS ON LUMINESCENCE IN VIBRIO HAR VEYI

机译：SAM相关结构和调节蛋白对哈维弧菌发光的影响

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摘要

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.
机译：哈维氏弧菌的发光诱导取决于自动诱导子的产生，该自动诱导子参与通过中央调节器LuxO参与复杂的信号转导系统。 SAM是生物系统中所需的关键代谢产物之一，并且在控制哈维弧菌发光的群体感应系统中，在两种自动诱导剂（AI-1和AI-2）的形成中起着核心作用。据信AI-1，N-羟基丁酰基高丝氨酸内酯是由SAM和由LuxM催化的N-羟基丁酰基-ACP的反应产生的。有确凿的证据表明AI-2是由SAM裂解为S-腺苷高半胱氨酸，然后裂解为S-核糖基同型半胱氨酸，然后被LuxS转化为核糖基衍生物，然后环化成呋喃酮。因此，我们预测限制SAM水平的基因应抑制发光，而刺激其合成的基因应减少发光。最近，我们发现参与SAM的调控和代谢的蛋白质极大地影响了哈维伊弧菌自身诱导物缺陷型突变体的发光水平。由于这些蛋白质可能与SAM和/或蛋氨酸（Met）的合成和降解有关，因此阐明这些蛋白质影响发光的机制的研究包括对自动感应因子水平和群体感应系统中涉及的其他调控元件的潜在影响。最重要的。这些研究应被证明对确定负责自诱导物合成的控制和特定途径具有重要意义。

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