Leyden M F, Schoeffel K L, MacPhee D G
Mutat Res. 1981 Dec;84(2):247-55. doi: 10.1016/0027-5107(81)90194-9.
Enhanced yields of UV-induced back mutants to prototrophy are observed when irradiated cells of the Salmonella typhimurium frameshift strain LT2 hisC3076 (R46) are plated on defined medium containing broth (2.5%, v/v) rather than a trace (0.2 micrograms/ml) of the required nutrient (histidine). This broth effect is not abolished, and is in fact augmented, in an excision-deficient derivative of hisC3076 (R46) carrying the uvr-302 mutation. Since similar broth effects on UV-induced base-pair substitution mutagenesis have usually been attributed to inhibition of mutation frequency decline (MFD), and since MFD is in turn thought to reflect the activity of an intact excision-repair system, we sought to determine whether or not UV-induced pre-mutational lesions leading to the production of frameshifts are susceptible to MFD. Results with the double auxotrophic strain LT2 hisC3076 leuA150 (pKM101) showed that in a population of cells actually undergoing MFD (as judged by a rapid loss of UV-induced reversions of the base-pair substitution marker leuA150), no concomitant loss of UV-induced reversions of the frameshift hisC3076 marker could be detected.
当将鼠伤寒沙门氏菌移码菌株LT2 hisC3076（R46）经紫外线照射后的细胞接种在含有肉汤（2.5%，v/v）而非痕量（0.2微克/毫升）所需营养物（组氨酸）的限定培养基上时，可观察到紫外线诱导的回复突变为原养型的产量增加。在携带uvr - 302突变的hisC3076（R46）的切除缺陷衍生物中，这种肉汤效应并未消除，实际上反而增强了。由于对紫外线诱导的碱基对置换诱变的类似肉汤效应通常归因于对突变频率下降（MFD）的抑制，并且由于MFD又被认为反映了完整切除修复系统的活性，我们试图确定导致移码产生的紫外线诱导的突变前损伤是否易受MFD影响。双营养缺陷型菌株LT2 hisC3076 leuA150（pKM101）的结果表明，在实际经历MFD的细胞群体中（通过碱基对置换标记leuA150的紫外线诱导回复突变的快速丧失来判断），未检测到移码hisC3076标记的紫外线诱导回复突变的伴随丧失。
