Hass B S, Webb R B
Mutat Res. 1979 Mar;60(1):1-11. doi: 10.1016/0027-5107(79)90204-5.
In the presence of acridine orange (AO) and monochromatic 500-nm light, the recombination-deficient strain of Escherichia coli, WP10 (recA), showed a 15-fold increase in mutation rate over the wild-type (WP2) strain. Under the same conditions, strain Bs--1 (uvrB lexA lon) showed a 5-fold increase in mutation rate over strain WP2. In contrast, the endonuclease-deficient, strain, WP2s (uvrA), showed a lower AO-500 nm mutation rate than wild-type. The extremely high mutation rate of the recA strain cannot be due to error-prone inducible SOS repair since the inducible recA + function is absent. Repair of the AO-500 nm-induced lesions is likely due to a recA+-dependent, error-free, recombination process. It is concluded that the high mutation rates with AO-500 nm light obtained in chemostat cultures of recA and lexA strains occur as a consequence of errors during semi-conservative DNA replication in the presence of unrepaired DNA lesions.
在吖啶橙(AO)和500纳米单色光存在的情况下,大肠杆菌的重组缺陷菌株WP10(recA)的突变率比野生型(WP2)菌株高出15倍。在相同条件下,Bs - 1菌株(uvrB lexA lon)的突变率比WP2菌株高出5倍。相比之下,内切核酸酶缺陷菌株WP2s(uvrA)的AO - 500纳米突变率低于野生型。recA菌株极高的突变率不可能归因于易错的诱导型SOS修复,因为不存在诱导型recA +功能。AO - 500纳米诱导损伤的修复可能是由于依赖recA +的无差错重组过程。得出的结论是,在recA和lexA菌株的恒化器培养物中,用AO - 500纳米光获得的高突变率是在存在未修复的DNA损伤时半保留DNA复制过程中出现错误的结果。