Carper S W, Duffy J J, Gerner E W
Department of Radiation Oncology, University of Arizona Health Sciences Center, Tucson 85724.
Cancer Res. 1987 Oct 15;47(20):5249-55.
Heat shock proteins appear to be causatively involved in the acquisition of thermotolerance in prokaryotes but not in eukaryotes. Further, the enhanced synthesis of hsps may be necessary for some cellular responses to stress but not others. In prokaryotic cells the development of thermotolerance, as measured by cell survival, is dependent upon protein synthesis. However, in eukaryotes, enhanced hsp synthesis following an inducing stress and prior to a subsequent heat shock is neither necessary nor sufficient for the development of thermotolerance as measured by colony-forming assays. The enhanced expression of hsps may be required for some mammalian cellular stress responses, such as the ability to reform both actin microfilament bundles and nucleolar morphology. These latter two thermotolerant responses have not been correlated with colony-forming ability. Future work should address the relationships between these various physiological responses to stress and determine if hsps function in some repair mode with regard to colony formation responses. Evidence is accumulating that hsps or their cognates may function in growth and differentiation in some manner as yet to be fully explained. Recent studies indicate that genes controlling cell division in E. coli may be linked to those of several stress regulons, and it would not be surprising to find a similar relationship in eukaryotes. At this time, it is important that studies investigating the role of hsps in stress and other cellular responses such as growth and differentiation define the specific gene (including its regulatory sequences) that encodes the protein being investigated, in order to avoid apparently contradictory and confusing reports of hsps expression.
热休克蛋白似乎在原核生物耐热性的获得中起因果作用，但在真核生物中并非如此。此外，热休克蛋白的合成增强对于某些细胞应激反应可能是必要的，但对其他反应则不然。在原核细胞中，通过细胞存活来衡量的耐热性发展依赖于蛋白质合成。然而，在真核生物中，诱导应激后及随后热休克之前热休克蛋白合成的增强，对于通过集落形成试验所衡量的耐热性发展既非必要条件也非充分条件。热休克蛋白的表达增强可能是某些哺乳动物细胞应激反应所必需的，比如重新形成肌动蛋白微丝束和核仁形态的能力。后两种耐热反应与集落形成能力并无关联。未来的工作应探讨这些不同的应激生理反应之间的关系，并确定热休克蛋白在集落形成反应方面是否以某种修复模式发挥作用。越来越多的证据表明，热休克蛋白或其同源物可能以某种尚未完全阐明的方式在生长和分化中发挥作用。最近的研究表明，大肠杆菌中控制细胞分裂的基因可能与几个应激调节子的基因相关联，在真核生物中发现类似的关系也不足为奇。目前，重要的是，研究热休克蛋白在应激及其他细胞反应（如生长和分化）中的作用时，要确定编码所研究蛋白质的特定基因（包括其调控序列），以避免出现关于热休克蛋白表达的明显矛盾和令人困惑的报告。
