SOS反應

SOS反應（SOS response）也稱應急反應，是對DNA損傷的整體反應，其中細胞周期被阻止，DNA修復和誘變被誘導。該系統涉及 RecA 蛋白（真核生物中的RAD51）。 RecA 蛋白受單鏈DNA刺激，參與SOS反應基因阻遏蛋白 (LexA) 的失活，從而誘導反應。它是一種容易出錯的修復系統，對在廣泛的物種中觀察到的 DNA 變化有重大貢獻。

E. coli SOS System: DNA can be damaged by cross-linking agents, UV irradiation, alkylating agents, etc. Once damaged, RecA, a LexA protease, senses that damaged DNA and becomes activated by removing its repressor. Once the LexA dimer repressor is removed, the expression of LexA operon is autoregulatory. In addition to being a LexA protease, the RecA protein also catalyzes a few novel DNA reactions such as annealing of single-stranded DNA and transfer of strands. The SOS system has enhanced DNA-repair capacity, including excision and post-replication repair, enhanced mutagenesis, prophage induction. The system can also inhibit cell division and cell respiration.

The SOS response has been proposed as a model for bacterial evolution of certain types of antibiotic resistance.

詳細機理

在正常生長過程中，SOS基因受到LexA抑制蛋白二聚體的抑制。在正常情況下，LexA與這些基因的操縱子區域20bp SOS box 結合。由於LexA 蛋白與SOS box 親和性差異，其中一些SOS基因即使在被中也以一定水平表達。當出現過多的單鏈DNA在複製叉處時，SOS基因的表達隨即被激活，複製叉處的DNA聚合酶解離，複製叉停止。

發現

由克羅埃西亞生物學家 Miroslav Radman 在1975年發現和命名，是指染色體DNA受到嚴重損傷時細胞做出的應激反應。在這種情況下，多種基因被誘導表達，其中1個拷貝的UmuC和2個拷貝的被截短的UmuD主要組成DNA聚合酶Ⅴ，後者可在DNA模板有切口的區域催化DNA複製。

參見

• DNA修復