三十年前Ritossa就报告热可引起果蝇唾液腺的染色体“疏松”。十年后发现由热引起的染色体疏松还伴有某些新蛋白—热休克蛋白(HSP)合成。几年后又发现热休克反应是很多种活细胞的内在特性:从细菌、真菌、植物、动物直至人类均可被包括热在内的各种“环境应激”所诱导。现在不仅知道HSP的基因结构与定位, 也了解该基因顺序在生物进化过程中高度保守。热刺激可使细胞在短时间内产生大量的HSP。在热休克中正常蛋白的合成被抑制;细胞回复到正常温度,抑制即被解除。热休克反应所需的温度有不同。在很宽的温度范围内均可生长的微生物(如大多数的真核生物),产生最强热休克反应的温度高于最适生长温度lO～ Thirty years ago Ritossa reported that heat can cause “looseness” in the chromosomes of the Drosophila salivary glands. Ten years later it was found that the heat-induced chromosomal looseness is accompanied by some new protein, heat shock protein (HSP) synthesis. A few years later, it was discovered that the heat shock response is inherent in many living cells: bacteria, fungi, plants, animals and even humans can be induced by a variety of “environmental stresses” including heat. Now not only know the gene structure and location of HSP, but also understand that the order of the gene in the biological evolution process is highly conservative. Thermal stimulation can make cells produce a large number of HSP in a short time. In heat shock normal protein synthesis is inhibited; cells returned to normal temperature, the inhibition is lifted. The temperature required for heat shock reactions varies. In a wide temperature range can grow microorganisms (such as most of the eukaryotes), produce the most intense heat shock reaction temperature is higher than the optimum growth temperature lO ~