Baltz R H, Stonesifer J
Mol Gen Genet. 1985;200(3):351-5. doi: 10.1007/BF00425716.
Two mutants of Streptomyces fradiae defective in DNA repair have been characterized for their responses to the mutagenic and lethal effects of several chemical mutagens and ultraviolet (UV) light. S. fradiae JS2 (mcr-2) was more sensitive than wild type to agents which produce bulky lesions resulting in large distortions of the double helix [i.e. UV-light, 4-nitroquinoline-1-oxide (NQO), and mitomycin C (MC)] but not to agents which produce small lesions [i.e. hydroxylamine (HA), methyl methanesulfonate (MMS), ethyl methanesulfonate (EMS) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)]. JS2 expressed a much higher frequency of mutagenesis induced by UV-light at low doses and thus appeared to be defective in an error-free excision repair pathway for bulky lesions analogous to the uvr ABC pathway of Escherichia coli. S. fradiae JS4 (mcr-4) was defective in repair of damage by most agents which produce small or bulky lesions (i.e., HA, NQO, MMS, MNNG, MC, and UV, but not EMS). JS4 was slightly hypermutable by EMS and MMS but showed reduced mutagenesis by NQO and HA. This unusual phenotype suggests that the mcr-4+ protein plays some role in error-prone repair in S. fradiae.
已对弗氏链霉菌的两个DNA修复缺陷型突变体对几种化学诱变剂和紫外线（UV）的诱变和致死效应的反应进行了表征。弗氏链霉菌JS2（mcr-2）比野生型对产生大的损伤导致双螺旋严重扭曲的试剂更敏感[即紫外线、4-硝基喹啉-1-氧化物（NQO）和丝裂霉素C（MC）]，但对产生小损伤的试剂不敏感[即羟胺（HA）、甲基磺酸甲酯（MMS）、乙基磺酸甲酯（EMS）和N-甲基-N'-硝基-N-亚硝基胍（MNNG）]。JS2在低剂量紫外线诱导下表现出更高的诱变频率，因此似乎在类似于大肠杆菌uvr ABC途径的针对大损伤的无差错切除修复途径中存在缺陷。弗氏链霉菌JS4（mcr-4）在修复由大多数产生小损伤或大损伤的试剂（即HA、NQO、MMS、MNNG、MC和UV，但不包括EMS）造成的损伤方面存在缺陷。JS4对EMS和MMS有轻微的超诱变作用，但对NQO和HA的诱变作用降低。这种不寻常的表型表明mcr-4+蛋白在弗氏链霉菌的易错修复中发挥了一定作用。
