Bridges B A
MRC Cell Mutation Unit, University of Sussex, Falmer, Brighton, UK.
Mutat Res. 1995 Jun;329(1):49-56. doi: 10.1016/0027-5107(95)00016-c.
When E. coli WU3610 (tyrA14 ochre) bacteria are starved of tyrosine on the surface of glucose-salts agar plates, there is a progressive accumulation of slow growing prototrophic mutants that are neither revertants at the ochre codon nor any of the well characterised tRNA ochre suppressors. Isogenic derivatives defective in transcription repair coupling factor (mfd) showed normal starvation-associated mutation (SAM). WU361045, the original mfd strain, showed very much reduced SAM. At 37 degrees C this was associated with progressive loss of viability on plates but the defect in SAM was not due to loss of viability since incubation at 27 degrees C or addition of catalase prevented the loss of viability but did not restore SAM. Furthermore, mutants could not be rescued from starved WU361045 populations by a short period of tyrosine supplementation arguing that WU361045 was defective not in the survival of starvation-associated mutants, but in their formation. The SAM defect in WU361045 was not complemented by the katF gene on a low copy number plasmid. It is concluded that WU361045 carries an unidentified mutation, not under katF control, that greatly reduces SAM. If SAM is attributable to a spontaneously occurring DNA lesion, the latter is unlikely to be formed by hydrogen peroxide or active species derived from it.
当大肠杆菌WU3610（tyrA14赭石型）细菌在葡萄糖 - 盐琼脂平板表面缺乏酪氨酸时，会逐渐积累生长缓慢的原养型突变体，这些突变体既不是赭石密码子的回复突变体，也不是任何已充分表征的tRNA赭石抑制子。转录修复偶联因子（mfd）有缺陷的同基因衍生物表现出正常的饥饿相关突变（SAM）。原始的mfd菌株WU361045表现出非常低的SAM。在37℃时，这与平板上活力的逐渐丧失有关，但SAM缺陷并非由于活力丧失，因为在27℃下培养或添加过氧化氢可防止活力丧失，但不能恢复SAM。此外，通过短时间补充酪氨酸无法从饥饿的WU361045群体中拯救突变体，这表明WU361045的缺陷不在于饥饿相关突变体的存活，而在于它们的形成。低拷贝数质粒上的katF基因不能互补WU361045中的SAM缺陷。得出的结论是，WU361045携带一种未鉴定的突变，不受katF控制，该突变大大降低了SAM。如果SAM归因于自发产生的DNA损伤，那么后者不太可能由过氧化氢或其衍生的活性物质形成。
