Puyo M F, Calsou P, Salles B
Laboratoire de Pharmacologie et Toxicologie Fondamentales CNRS, Toulouse, France.
Mutat Res. 1992 Aug;282(4):247-52. doi: 10.1016/0165-7992(92)90130-a.
Deletion of genes for adenylate cyclase (delta cya) or cAMP receptor protein (delta crp) in E. coli K-12 confers a phenotype that includes resistance to UV radiation (254 nm). Such mutations lead to UV resistance of uvr+, uvrA, lexA and recA strains which could partly be abolished by the addition of cAMP to delta cya but not to delta crp strain culture medium. This effect was not related to either inducibility of major DNA repair genes or growth rate of the bacteria. Enhanced survival was also observed for UV-irradiated lambda bacteriophage indicating that a repair mechanism of UV lesions was involved in this phenomenon.
在大肠杆菌K-12中缺失腺苷酸环化酶基因（delta cya）或cAMP受体蛋白基因（delta crp）会赋予一种表型，包括对紫外线辐射（254纳米）的抗性。此类突变导致uvr+、uvrA、lexA和recA菌株产生紫外线抗性，向delta cya菌株的培养基中添加cAMP可部分消除这种抗性，但向delta crp菌株的培养基中添加cAMP则无法消除。这种效应与主要DNA修复基因的诱导性或细菌的生长速率均无关。对于紫外线照射的λ噬菌体也观察到存活率提高，这表明紫外线损伤的修复机制参与了这一现象。
