Isolation and characterization of an Escherichia coli mutant defective in resuming growth after starvation.
Isolation and characterization of an Escherichia coli mutant defective in resuming growth after starvation.
复制标题
饥饿后恢复生长缺陷的大肠杆菌突变体的分离和表征。
DOI：
10.1101/gad.7.12b.2629
复制
发表时间：
1993
影响因子：
10.5
通讯作者：
Kolter,R
中科院分区：
文献类型：
--
作者：
Siegele,DA;Kolter,R
为了了解肠道细菌大肠杆菌的机制，使生长和稳定期之间的过渡，并在饥饿期间保持细胞活力，我们已经寻找突变体缺陷的稳定期生存（一个表面活性剂表型）。在本文中，我们描述了一个条件E。大肠杆菌突变株surB 1在稳定期内生长正常，但在高温下不能脱离稳定期，恢复需氧生长。因此，surB基因产物本身不是细胞存活所必需的，而是饥饿的细胞在限制性条件下重新开始生长所必需的。一旦开始生长，就不再需要SurB功能。突变细胞对新鲜培养基有感应和反应，但似乎在第一次细胞分裂前停止生长。surB基因在E. coli染色体，克隆并测序。surB基因产物被预测为具有多个跨膜区域的完整膜蛋白，并且与转运蛋白的ATP结合盒（ABC）家族同源，所述转运蛋白是在原核和真核细胞中发现的转运蛋白的大家族。紧邻surB上游发现了一个开放的阅读框架，命名为ybjA，并且可能位于surB的操纵子中。预测的ybjA基因产物也与ABC转运蛋白家族同源，并且SurB和YbjA可能在共同的转运途径中一起起作用。surB或ybjA可以是与cydC相同的基因，cydC是先前描述的基因，其功能是产生功能性细胞色素d氧化酶复合物所需的。与此预测一致，surB 1突变细胞被发现缺乏功能性细胞色素d氧化酶。然而，SurB-表型不是简单地归因于细胞色素d氧化酶的情况下。因此，surB基因产物可能在细胞中具有额外的作用。
To understand the mechanisms that allow the enteric bacterium Escherichia coli to make the transitions between growth and stationary phase and to maintain cell viability during starvation, we have looked for mutants defective in stationary-phase survival (a Sur-phenotype). In this paper we describe a conditional E. coli mutant, surB1, that grows normally and remains viable during stationary phase but is unable to exit stationary phase and resume aerobic growth at high temperature. Thus, the surB gene product is not required for cell survival per se but, rather, it is required for starved cells to reinitiate growth under restrictive conditions. Once growth has started, SurB function is no longer required. Mutant cells sense and respond to fresh medium but appear to arrest growth before the first cell division. The surB gene was mapped to 19.5 min on the E. coli chromosome, cloned, and sequenced. The surB gene product is predicted to be an integral membrane protein with multiple membrane-spanning regions and is homologous to the ATP-binding cassette (ABC) family of transporters, a large family of transport proteins found in both prokaryotic and eukaryotic cells. An open reading frame, designated ybjA, was found immediately upstream of surB and may be in an operon with surB. The predicted ybjA gene product is also homologous to the ABC transporter family and SurB and YbjA may function together in a common transport pathway. Either surB or ybjA may be the same gene as cydC, a gene described previously whose function is needed for the production of functional cytochrome d oxidase complexes. Consistent with this prediction, surB1 mutant cells were found to lack functional cytochrome d oxidase. However, the SurB-phenotype is not simply attributable to the absence of cytochrome d oxidase. Thus, the surB gene product may have an additional role in the cell.