A study of the topological change of DNA in Escherichia coli induced by heat shock.

热激诱导大肠杆菌DNA拓扑变化的研究。

• 批准号: 04680153
• 负责人: SEKIMIZU Kazuhisa
• 金额: $ 1.41万
• 依托单位: KYUSHU UNIVERSITY
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1992
• 资助国家: 日本
• 起止时间: 1992 至 1993
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-04680153/
• 关键词: DNA topology; DNA supercoiling; DNA topoisomerase; DNA gyrase; heat shock response; heat shock proteins; recombination; Escherichia coli; 熱ショック蛋白; 相同組み換え; DNA topology; DNA supercoiling; DNA topoisomerase; DNA gyrase; heat shock response; heat shock proteins; recombination; Escherichia coli; 熱ショック蛋白; 相同組み換え

Heat treatment of wild-type Escherichia coli cells leads to relaxation of negatively supercolied plasmid DNA, followed by a re-supercoiling reaction to the original level of the linking number of DNA.There was no evidence of the recovery of the DNA torsional strain in DNA of gyrA mutant cells. After heat treatment, DnaK and GroEL proteins were synthesized continuously in gyrA mutant cells but only transiently in wild-type cells. Thus, change in superhelical density of the DNA correlates with temperature -induced expression of heat shock proteins.Inhibitors of DNA gyrase (nalidixic acid, novobiocin), an organic solvent (ethanol) and a psychotropic drug (chlorpromazine) all stimulated relaxation of cellular DNA, over the same concentration range that induced DnaK and GroEL proteins, As DNA relaxation was induced by heat treatment or chemicals in an rpoH, mutant, the process is not the result of any induced synthesis of heat shock proteins.In rpoH and dnaK mutants, a re-supercoiling reaction did not occur, hence DnaK protein and other heat shock proteins presumably participate in the reaction. We propose that DNA relaxation induced by heat treatment stimulates synthesis of heat shock proteins involved in the re-supercoiling of DNA, which in turn shuts off the induction of these proteins.

野生型大肠杆菌细胞的热处理导致质溶解的质粒DNA的放松，然后对DNA连接数的原始水平进行重新固定反应。热处理后，在Gyra突变细胞中连续合成DNAK和GROEL蛋白，但仅在野生型细胞中暂时合成。因此，DNA的超固定密度的变化与温度诱导的热休克蛋白的表达相关。抑制剂DNA陀螺酶（Nalidixic，Novobiocin，Novobiocin），有机溶剂溶剂（乙醇）和精神药物（氯丙嗪）均刺激了相同的浓度，这些浓缩范围都与persular dna相同，并指出了同一浓缩范围，并指出了DN的繁殖率，并指出了DNA的繁殖。在RPOH，突变体中通过热处理或化学物质诱导该过程并不是任何诱导的热休克蛋白合成的结果。在RPOH和DNAK突变体中，没有发生重新固定反应，因此DNAK蛋白和其他热休克蛋白可能参与了反应。我们提出，热处理诱导的DNA弛豫刺激了与DNA重新固定的热激蛋白的合成，进而关闭了这些蛋白质的诱导。