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铜绿假单胞菌的磷脂酶C调节突变,导致几种磷酸盐阻遏蛋白的组成型合成。

Phospholipase C regulatory mutation of Pseudomonas aeruginosa that results in constitutive synthesis of several phosphate-repressible proteins.

作者信息

Gray G L, Berka R M, Vasil M L

出版信息

J Bacteriol. 1982 Jun;150(3):1221-6. doi: 10.1128/jb.150.3.1221-1226.1982.

Abstract

We describe here a new mutant of Pseudomonas aeruginosa PAO, strain D10C (genotype plcB), which produces phospholipase C and alkaline phosphatase constitutively. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of the extracellular proteins produced by this mutant in high- and low-Pi media revealed that the mutation resulted in a marked deficiency of one major Pi-regulated protein of 41,000 molecular weight and constitutive synthesis of all other major extracellular Pi-regulated proteins. Furthermore, the plcB mutant was deficient in phosphate transport. A plcA mutation, which also led to a loss of the 41,000-molecular-weight protein, was similarly deficient in Pi transport. The genetic loci, plcA and plcB, located at 22 to 23 min on the PAO chromosome, were indistinguishable by conjugational and transductional mapping, and may therefore be in the same gene or in a cluster of genes which regulate the synthesis of Pi-repressible proteins.

摘要

我们在此描述铜绿假单胞菌PAO的一个新突变体,菌株D10C(基因型plcB),其组成型产生磷脂酶C和碱性磷酸酶。该突变体在高磷和低磷培养基中产生的细胞外蛋白的十二烷基硫酸钠-聚丙烯酰胺凝胶电泳显示,该突变导致一种分子量为41,000的主要磷调节蛋白明显缺乏,而所有其他主要细胞外磷调节蛋白则组成型合成。此外,plcB突变体在磷酸盐转运方面存在缺陷。plcA突变同样导致41,000分子量蛋白的缺失,在磷转运方面也同样存在缺陷。位于PAO染色体22至23分钟处的基因座plcA和plcB,通过接合和转导图谱分析无法区分,因此可能位于同一基因或调节磷抑制蛋白合成的基因簇中。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/619c/216343/9fbf1a992584/jbacter00259-0235-a.jpg

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