EXPRESSION AND ROLE OF THE UNIVERSAL STRESS PROTEIN, USPA, OF ESCHERICHIA-COLI DURING GROWTH ARREST
EXPRESSION AND ROLE OF THE UNIVERSAL STRESS PROTEIN, USPA, OF ESCHERICHIA-COLI DURING GROWTH ARREST
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DOI：
10.1111/j.1365-2958.1994.tb00334.x
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发表时间：
1994-02-01
影响因子：
3.6
通讯作者：
NEIDHARDT, FC
中科院分区：
文献类型：
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作者：
NYSTROM, T;NEIDHARDT, FC
无论抑制生长的条件如何，只要细胞生长速率福尔斯低于培养基支持的最大生长速率，大肠杆菌的小细胞质蛋白UspA（通用应激蛋白A）的合成就被诱导。UspA合成的增加似乎是单顺反子uspA基因诱导的结果。在热休克处理过程中该基因的诱导被证明是sigma（70）依赖性启动子的转录激活的结果，该启动子先前已被证明在碳饥饿诱导的生长停滞过程中也被激活。缺乏UspA的突变体细胞在不同的温度和不同的生长抑制剂的存在下，以与同基因亲本不可替代的速率生长，但是它们在由各种不同的应激（包括CdCl 2、H2O2 DNP、CCCP暴露和渗透压休克）引起的长时间完全生长抑制中存活的能力受损。此外，uspA突变导致细胞对碳源饥饿（即葡萄糖、甘油或琥珀酸耗尽）的敏感性增加。此外，突变导致饥饿蛋白表达的时间发生显着改变，但在稳态生长期间的蛋白表达似乎是正常的。这些结果促使我们推测UspA可能具有与生长停滞状态相关的一般保护功能。
The synthesis of the small, cytoplasmic protein UspA universal stress protein A) of Escherichia coli is induced as soon as the cell growth rate falls below the maximal growth rate supported by the medium, regardless of the condition inhibiting growth. The increase in UspA synthesis appears to be the result of induction of the monocistronic uspA gene. Induction of this gene during a heat-shock treatment is demonstrated to be the result of transcriptional activation of a sigma(70)-dependent promoter which has previously been shown to be activated also during carbon starvation-induced growth arrest. Mutant cells lacking UspA grow at rates indistinguisible from the isogenic parent at different temperatures and in the presence of different growth inhibitors but are impaired in their ability to survive prolonged periods of complete growth inhibition caused by a variety of diverse stresses, including CdCl2, H2O2 DNP, CCCP exposure, and osmotic shock. Moreover, the uspA mutation results in an increased sensitivity of cells to carbon-source starvation (i.e. glucose, glycerol or succinate depletion). Also, the mutation causes a marked alteration in the timing of starvation protein expression but protein expression during steady-state growth appears to be normal. The results presented have prompted us to postulate that UspA may have a general protective function related to the growth arrest state.