【摘要】 假单胞菌株M18分泌藤黄绿脓菌素 (Pyoluteorin ,Plt )和吩嗪 1 羧酸 (Phenazine 1 carboxylicacid ,PCA)并抑制多种植物病菌的生长。从M18中克隆双基因调控系统gacS gacA的组成基因gacA ,并构建了该基因抗性插入突变株M18G。在KMB培养基中 ,M18G合成Plt的能力受到完全抑制 ,而PCA的积累约比野生型提高 31倍左右。Plt合成基因簇突变株M18T和在M18G基础上构建的PCA合成基因簇突变株M18GA的Plt和PCA合成的动力学变化表明 ,在M18G菌株中 ,Plt合成的抑制并不引起PCA的过量积累 ,PCA的过量积累也不引起Plt合成的抑制。由此推测 ,gacA在基因表达的水平上全局性地执行着调控功能更多还原

【Abstract】 Pseudomonas sp. M18 is one of the plant-growth-promoting rhizobacteria, which can produce fungicides: phenazine-1-carboxylic acid (PCA) and pyoluteorin (Plt). The chromosomally gacA inactivated mutant named M18G was constructed and its PCA production was enhanced 31-fold and Plt production was almost blocked completely in KMB medium. To assess the mutual influence of two antibiotics, the plt gene cluster mutant M18T and the phz gene cluster mutant M18GA were then constructed. Non-Plt-producing M18T could synthesize the same amount of PCA as wild type strain. Plt could not be detected in M18GA while PCA production was inhibited dramatically in it. Results indicate that promotion of PCA and inhibition of Plt production in M18G do result from the inactivation of gacA gene. It suggests that the production of antibiotics in strain M18 is differentially mediated by the gacA.更多还原