Eisenstark A, Calcutt M J, Becker-Hapak M, Ivanova A
Cancer Research Center, University of Missouri, Columbia, USA.
Free Radic Biol Med. 1996;21(7):975-93. doi: 10.1016/s0891-5849(96)00154-2.
The first phenotype described for mutations in the Escherichia coli rpoS gene was hypersensitivity to near-ultraviolet radiation and to its oxidative photoproduct, hydrogen peroxide. Initially named nur, this gene is now known to code for a sigma factor, and has acquired new names such as katF and rpoS. The role of its protein product (sigma-38) is to regulate a battery of genes as cells enter and rest in stationary phase. Some of the gene products are involved in protection against oxidants (e.g., catalases) and repair of oxidative damage (e.g., exonuclease III). Sigma-38 may also modulate transcription of certain growth phase genes, including hydroperoxidase I and glutathione reductase. Sigma-38 activity is regulated at transcriptional, translational, and protein stabilization levels. This review describes the complex mechanisms whereby sigma-38 controls various genes, the interaction of sigma-38 with other regulators, and a possible role of sigma-38 in bacterial virulence.
大肠杆菌rpoS基因突变所描述的首个表型是对近紫外辐射及其氧化光产物过氧化氢高度敏感。该基因最初名为nur,现在已知它编码一种σ因子,并获得了katF和rpoS等新名称。其蛋白质产物(σ-38)的作用是在细胞进入稳定期并处于稳定期时调控一系列基因。一些基因产物参与抗氧化剂防御(如过氧化氢酶)和氧化损伤修复(如核酸外切酶III)。σ-38还可能调节某些生长阶段基因的转录,包括氢过氧化物酶I和谷胱甘肽还原酶。σ-38的活性在转录、翻译和蛋白质稳定水平上受到调控。本综述描述了σ-38控制各种基因的复杂机制、σ-38与其他调节因子的相互作用以及σ-38在细菌毒力中可能发挥的作用。