Hansen M T
J Bacteriol. 1980 Jan;141(1):81-6. doi: 10.1128/jb.141.1.81-86.1980.
Four proteins, alpha beta, gamma, and delta, preferentially synthesized in ultraviolet light-treated cells of Micrococcus radiodurans, were characterized in terms of their molecular weights and isoelectric points. Within the sublethal-dose range, the differential rate of synthesis for these proteins increased linearly with the inducing UV dose. The degree of induction reached 100-fold, and the most abundant protein beta, amounted to approximately 2% of the total newly synthesized protein after irradiation. Damage caused by ionizing radiation or by treatment with mitomycin C also provoked the synthesis of the four proteins. The proportions between the individual proteins, however, varied strikingly with the damaging agent. In contrast to treatments which introduced damage in the cellular deoxyribonucleic acid, the mere arrest of deoxyribonucleic acid replication, caused by nalidixic acid or by starvation for thymine, failed to elicit the synthesis of either protein. Repair of deoxyribonucleic acid damage requires that a number of versatile and efficient processes by employed. It is proposed that the induced proteins participate in deoxyribonucleic acid repair in M. radiodurans. Mechanisms are discussed which would allow a differentiated cellular response to damages of sufficiently distinctive nature.
在经紫外线处理的耐辐射微球菌细胞中优先合成的四种蛋白质,即α、β、γ和δ,根据其分子量和等电点进行了表征。在亚致死剂量范围内,这些蛋白质的合成差异率随诱导紫外线剂量呈线性增加。诱导程度达到100倍,最丰富的蛋白质β在照射后占新合成蛋白质总量的约2%。电离辐射或丝裂霉素C处理造成的损伤也会引发这四种蛋白质的合成。然而,单个蛋白质之间的比例因损伤剂的不同而有显著差异。与在细胞脱氧核糖核酸中造成损伤的处理不同,由萘啶酸或胸腺嘧啶饥饿导致的脱氧核糖核酸复制的单纯停滞未能引发任何一种蛋白质的合成。脱氧核糖核酸损伤的修复需要采用许多通用且高效的过程。有人提出,诱导产生的蛋白质参与了耐辐射微球菌的脱氧核糖核酸修复。文中讨论了能够使细胞对具有足够独特性质的损伤产生分化反应的机制。