CELLULAR DEFECTS CAUSED BY DELETION OF THE ESCHERICHIA-COLI DNAK GENE INDICATE ROLES FOR HEAT-SHOCK PROTEIN IN NORMAL METABOLISM
CELLULAR DEFECTS CAUSED BY DELETION OF THE ESCHERICHIA-COLI DNAK GENE INDICATE ROLES FOR HEAT-SHOCK PROTEIN IN NORMAL METABOLISM
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DOI：
10.1128/jb.171.5.2337-2346.1989
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发表时间：
1989-05-01
影响因子：
3.2
通讯作者：
WALKER, GC
中科院分区：
文献类型：
--
作者：
BUKAU, B;WALKER, GC
DnaK是大肠杆菌的主要热休克蛋白，并且先前已报道对于在高温下的生长是必需的。我们通过分析由dnaK基因（Δ dnaK 52）缺失引起的细胞缺陷，系统地研究了DnaK在宽范围生长温度下的细胞代谢中的作用。在中间温度（30 ℃）下，C），将Δ dnaK 52导入野生型细胞引起细胞分裂的严重缺陷、生长缓慢和细胞活力差，Δ dnaK 52突变体在30 ℃下遗传不稳定。C和经常获得的继发性突变。高（42度）C）和低（11和16. C）温度下，Δ dnaK 52等位基因只能被引入到已经复制了其染色体的dnaK区域的野生型细胞亚群中。在30 ℃分离Δ dnaK 52突变体。C是冷敏感的，以及温度敏感的生长。Δ dnaK 52突变体在30 ℃的细胞分裂缺陷C在很大程度上被FtsZ蛋白的过量产生所抑制，FtsZ蛋白通常是细胞分裂期间分隔所需的;然而，在30 ℃下生长缓慢且存活力差。生长的C和冷敏感性和温度敏感性没有被抑制，表明Δ dnaK 52突变体除了细胞分裂之外还具有另外的缺陷功能。
DnaK is a major heat shock protein of Escherichia coli and has been previously reported to be essential for growth at high temperatures. We systematically investigated the role of DnaK in cellular metabolism at a wide range of growth temperatures by analyzing cellular defects caused by deletion of the dnaK gene (.DELTA.dnaK52). At intermediate temperatures (30.degree. C), introduced of the .DELTA.dnaK52 into wild-type cells caused severe defects in cell division, slow growth, and poor viability of the cells, .DELTA.dnaK52 mutants were genetically unstable at 30.degree. C and frequently acquired secondary mutations. At high (42.degree. C) and low (11 and 16.degree. C) temperatures the .DELTA.dnaK52 allele could only be introduced into the subpopulation of wild-type cells that had duplicated the dnaK region of their chromosome. .DELTA.dnaK52 mutants isolated at 30.degree. C were cold sensitive as well as temperature sensitive for growth. Cell division defects of .DELTA.dnaK52 mutants at 30.degree. C were largely suppressed by overproduction of the FtsZ protein, which is normally required for septation during cell division; however, slow growth and poor viability at 30.degree. C and cold sensitivity and temperature sensitivity of growth were not suppressed, indicating that .DELTA.dnaK52 mutants had additional defective functions besides cell division.