首页> 美国卫生研究院文献>Journal of Bacteriology >Mutation of a Gene Encoding a Putative Glycoprotease Leads to Reduced Salt Tolerance Altered Pigmentation and Cyanophycin Accumulation in the Cyanobacterium Synechocystis sp. Strain PCC 6803
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Mutation of a Gene Encoding a Putative Glycoprotease Leads to Reduced Salt Tolerance Altered Pigmentation and Cyanophycin Accumulation in the Cyanobacterium Synechocystis sp. Strain PCC 6803

机译:编码假定的糖蛋白的基因的突变会导致蓝藻蓝藻中耐盐性下降色素沉着改变和蓝霉素积累。应变PCC 6803

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摘要

The salt-sensitive mutant 549 of the cyanobacterium Synechocystis sp. strain PCC 6803 was genetically and physiologically characterized. The mutated site and corresponding wild-type site were cloned and partially sequenced. The genetic analysis revealed that during the mutation about 1.8 kb was deleted from the chromosome of mutant 549. This deletion affected four open reading frames: a gcp gene homolog, the psaFJ genes, and an unknown gene. After construction of mutants with single mutations, only the gcp mutant showed a reduction in salt tolerance comparable to that of the initial mutant, indicating that the deletion of this gene was responsible for the salt sensitivity and that the other genes were of minor importance. Besides the reduced salt tolerance, a remarkable change in pigmentation was observed that became more pronounced in salt-stressed cells. The phycobilipigment content decreased, and that of carotenoids increased. Investigations of changes in the ultrastructure revealed an increase in the amount of characteristic inclusion bodies containing the high-molecular-weight nitrogen storage polymer cyanophycin (polyaspartate and arginine). The salt-induced accumulation of cyanophycin was confirmed by chemical estimations. The putative glycoprotease encoded by the gcp gene might be responsible for the degradation of cyanophycin in Synechocystis. Mutation of this gene leads to nitrogen starvation of the cells, accompanied by characteristic changes in pigmentation, ultrastructure, and salt tolerance level.
机译:蓝藻Synechocystis sp。的盐敏感性突变体549。对PCC 6803菌株进行了遗传和生理学表征。克隆突变位点和相应的野生型位点并部分测序。遗传分析表明,在突变期间,突变体549的染色体中缺失了约1.8 kb。这种缺失影响了四个开放阅读框:一个gcp基因同源物,psaFJ基因和一个未知基因。构建具有单个突变的突变体后,只有gcp突变体显示出与初始突变体相当的耐盐性降低,表明该基因的缺失是造成盐敏感性的原因,而其他基因则次要。除了降低了耐盐性外,还观察到色素沉着的显着变化,在盐胁迫细胞中变得更加明显。藻胆色素含量降低,而类胡萝卜素含量升高。对超微结构变化的研究表明,包含高分子量氮存储聚合物氰霉素(聚天冬氨酸和精氨酸)的特征包涵体的数量有所增加。通过化学估计证实了盐诱导的氰霉素积累。 gcp基因编码的推定的糖蛋白酶可能是导致集胞藻中蓝霉素降解的原因。该基因的突变导致细胞的氮饥饿,伴随着色素沉着,超微结构和耐盐性水平的特征性变化。

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