首页> 外文OA文献 >A New GntR Family Transcriptional Regulator in Streptomyces coelicolor Is Required for Morphogenesis and Antibiotic Production and Controls Transcription of an ABC Transporter in Response to Carbon Source▿
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A New GntR Family Transcriptional Regulator in Streptomyces coelicolor Is Required for Morphogenesis and Antibiotic Production and Controls Transcription of an ABC Transporter in Response to Carbon Source▿

机译:天蓝色链霉菌中新的GntR家族转录调节剂是形态发生和抗生素生产所必需的,并能响应碳源控制ABC转运蛋白的转录。

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摘要

We recently reported the isolation and initial characterization of a transposon-generated mutation that resulted in defects in both morphogenesis and antibiotic production in Streptomyces coelicolor. The insertion identified the SCO7168 open reading frame whose predicted product is a GntR family transcriptional regulator. Here, we show that this gene acts to repress transcription of itself as well as a series of genes immediately adjacent to it on the S. coelicolor chromosome that likely encode an ATP-binding cassette (ABC)-type transporter for carbohydrate uptake. Transcription of this transporter is strongly induced by growth on relatively poor carbon sources such as trehalose and melibiose and weakly induced by lactose and glycerol but not glucose, and induction is not repressed by the presence of glucose. Constructed deletions of the ABC transporter itself resulted in the suppression of the original transposon mutation, suggesting that inappropriate expression of the ABC transporter is responsible, at least in part, for the mutant phenotype. Because this transporter responds to the presence of α-glucosides and has similarity to two other carbohydrate transporters of this class, we have named the genes of the transporter agl3E, agl3F, and agl3G and the GntR-like protein that regulates transcription of the transporter agl3R in accordance with established nomenclature. We suggest that agl3R is one of a number of homologous proteins in Streptomyces (there are 57 putative GntR family regulators in the S. coelicolor genome) that respond to nutritional and/or environmental signals to control genes that affect morphogenesis and antibiotic production.
机译:我们最近报道了转座子产生的突变的分离和初步表征,该突变导致天蓝色链霉菌的形态发生和抗生素生产均存在缺陷。该插入识别出SCO7168开放阅读框,其预测产物是GntR家族转录调节子。在这里,我们显示该基因可抑制其自身以及一系列与其紧密相关的基因的转录,这些基因可能会编码天蓝色链霉菌染色体,该基因可能编码碳水化合物吸收的ATP结合盒(ABC)型转运蛋白。该转运蛋白的转录在相对较弱的碳源(如海藻糖和蜜三糖)上生长而强烈诱导,而乳糖和甘油而不是葡萄糖则弱诱导,并且葡萄糖的存在不抑制诱导。 ABC转运蛋白本身的构建的缺失导致原始转座子突变的抑制,这表明ABC转运蛋白的不适当表达至少部分是造成突变表型的原因。由于该转运蛋白对α-葡萄糖苷的存在做出反应,并且与该类其他两种碳水化合物转运蛋白具有相似性,因此我们将转运蛋白agl3E,agl3F和agl3G的基因命名为GntR样蛋白,该蛋白调节转运蛋白agl3R的转录按照既定命名法。我们建议,agl3R是链霉菌中的许多同源蛋白之一(在天蓝色链霉菌基因组中有57个假定的GntR家族调节剂),它们响应营养和/或环境信号来控制影响形态发生和抗生素生产的基因。

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