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从肺炎克雷伯菌中分离并鉴定出两个激活大肠杆菌中柯氏酸荚膜生物合成的rcs基因。

Isolation from Klebsiella and characterization of two rcs genes that activate colanic acid capsular biosynthesis in Escherichia coli.

作者信息

Allen P, Hart C A, Saunders J R

机构信息

Department of Microbiology, University of Liverpool, UK.

出版信息

J Gen Microbiol. 1987 Feb;133(2):331-40. doi: 10.1099/00221287-133-2-331.

DOI:10.1099/00221287-133-2-331
PMID:3309150
Abstract

Two genes, designated rcsA (regulation of capsule synthesis) and rcsB, that had been cloned from the chromosome of Klebsiella aerogenes (K. pneumoniae) capsular serotype K21 were capable of activating expression of colanic acid capsular polysaccharide in Escherichia coli K12. The Klebsiella rcsA gene encoded a polypeptide of 23 kDa that was required for the induction of a mucoid phenotype at less than or equal to 30 degrees C but not at greater than or equal to 37 C. The Klebsiella rcsB locus encoded no apparent polypeptides and was not capable by itself of causing the overproduction of colanic acid. However, when present in the same cell with rcsA, either in cis or in trans, rcsB caused expression of mucoidy in E. coli at all growth temperatures. These findings are best explained if the Klebsiella rcsA gene product acts as a positive regulator of colanic acid biosynthesis in E. coli and that activity of this protein is in turn subject to regulation by Lon protease. The Klebsiella rcsB locus may exert its effect by preferentially binding a negative regulator of capsular biosynthesis, possibly Lon itself. DNA sequences homologous to the Klebsiella K21b rcsA and rcsB genes were found in the genomes of all other capsular serotypes of klebsiellae examined, including K2, K12, K36 and K43. However, there was no homology between such genes and the chromosome of E. coli. The ability of these rcs genes to induce a mucoid phenotype explains the apparent conjugative transfer from klebsiellae to E. coli of the ability to produce K21 or other Klebsiella capsular polysaccharides that are structurally and antigenically related to colanic acid.

摘要

从产气克雷伯菌(肺炎克雷伯菌)荚膜血清型K21染色体上克隆出的两个基因,分别命名为rcsA(荚膜合成调节基因)和rcsB,能够激活大肠杆菌K12中结肠酸荚膜多糖的表达。克雷伯菌的rcsA基因编码一种23 kDa的多肽,该多肽在小于或等于30℃时是诱导黏液样表型所必需的,但在大于或等于37℃时则不是。克雷伯菌的rcsB位点不编码明显的多肽,其自身也不能导致结肠酸的过量产生。然而,当rcsB与rcsA存在于同一细胞中时,无论是顺式还是反式,rcsB都会在所有生长温度下使大肠杆菌中出现黏液样表型。如果克雷伯菌的rcsA基因产物作为大肠杆菌中结肠酸生物合成的正调控因子,且该蛋白的活性又受到Lon蛋白酶的调控,那么这些发现就能得到最好的解释。克雷伯菌的rcsB位点可能通过优先结合荚膜生物合成的负调控因子(可能是Lon自身)来发挥其作用。在所有检测的克雷伯菌其他荚膜血清型(包括K2、K12、K36和K43)的基因组中都发现了与克雷伯菌K21b的rcsA和rcsB基因同源的DNA序列。然而,这些基因与大肠杆菌的染色体之间没有同源性。这些rcs基因诱导黏液样表型的能力解释了从克雷伯菌到大肠杆菌的明显的接合转移,即产生与结肠酸在结构和抗原性上相关的K21或其他克雷伯菌荚膜多糖的能力。

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