Aĭzenberg O A, Samoĭlenko I I, Fradkin G E
Genetika. 1977;13(11):1988-96.
Thymine requiring mutants of rec+ and recB- Escherichia coli strains have been tested for their response to thymine deprivation. Exonuclease V-deficient mutant is less sensitive to thymine deprivation than the wild type strain, because there is no lag period at thymineless death of recB- thy- cells. However, the mechanism of thymineless death of thy- rec+ and thy- recB- cells may be different. Two types of thymineless death are proposed to exist. The first type is due to DNA primary structure damages (single-strand breaks or gaps), accompanied by DNA degradation. The restoration of the balance disturbed by the thymine deprivation between DNA and protein synthesis rates by their balanced inhibition promotes a complete repair of structural damages in DNA and prevents the death of rec+ cells. The second type of thymineless death is not linked with the formation of DNA damages, and this is observed in recB- thy- mutant, defective in exonuclease V.
已对rec⁺和recB⁻大肠杆菌菌株的胸腺嘧啶需求型突变体进行测试,以观察它们对胸腺嘧啶剥夺的反应。核酸外切酶V缺陷型突变体对胸腺嘧啶剥夺的敏感性低于野生型菌株,因为recB⁻ thy⁻细胞在胸腺嘧啶饥饿死亡时没有延迟期。然而,thy⁻ rec⁺和thy⁻ recB⁻细胞的胸腺嘧啶饥饿死亡机制可能不同。有人提出存在两种类型的胸腺嘧啶饥饿死亡。第一种类型是由于DNA一级结构损伤(单链断裂或缺口),伴有DNA降解。通过平衡抑制来恢复胸腺嘧啶剥夺所扰乱的DNA与蛋白质合成速率之间的平衡,可促进DNA结构损伤的完全修复,并防止rec⁺细胞死亡。第二种类型的胸腺嘧啶饥饿死亡与DNA损伤的形成无关,这在核酸外切酶V缺陷的recB⁻ thy⁻突变体中观察到。