利福平诱导rpoB基因突变活化变青链霉菌66合成放线紫红素

Activated actinorhodin production in Streptomyces lividans 66 by inducing rifampicin-resistant mutations

变青链霉菌拥有完整的放线紫红素生物合成基因簇 ,但它通常并不合成这一抗生素。引入特定的rpoB基因 ,不仅产生了对利福平的抗性 ,同时活化了放线紫红素的合成 ,表明由该基因编码的RNA聚合酶 β亚基因在抗生素的生物合成调控中起十分重要的作用。DNA顺序分析揭示出在rpoB基因上的四种不同突变类型 ,均不同程度地活化变青链霉菌合成放线紫红素 ,表明利福平具有与链霉素类似的功能 ,即活化或加强链霉菌合成抗生素或酶的水平。

Streptomyces lividans 66 does not produce actinorhodin under normal conditions in spite of the whole actinorhodin biosynthetic gene cluster. By inducing specific mutations in the rpoB gene of Streptomyces lividans 66, resistance to rifampicin and activated actinorhodin production in Streptomyces lividans 66 occurred. This indicated that the rpoB gene encoding β subunit of RNA polymerase plays an important role in regulating antibiotic biosynthesis in Streptomyces . DNA sequencing analysis revealed that four kinds of point mutations appeared in these mutants, and exhibited different abilities to activate actinorhodin production. These results suggested that rifampicin , like streptomycin, could be used to activate or enhance antibiotic biosynthesis in Streptomyces .