Savić D J, Romac S P
J Bacteriol. 1982 Mar;149(3):955-60. doi: 10.1128/jb.149.3.955-960.1982.
We examined 122 spontaneous histidine auxotrophs accumulated in overnight cultures of polA1 strains of Escherichia coli K-12 at approximate frequencies of 10(-3). One hundred and thirteen appeared to be minus frameshifts, and nine appeared to be deletions. Of the frameshift mutations, 109 affected the hisC gene, and 4 affected genes hisD, hisH, hisA, and hisI. The lack of base substitutions supported the idea that polymerase-defective polA is a minus frameshift- and deletion-type mutator. Contrary to a previous report, we did not observe superior growth of PolA auxotrophs over their prototrophic progenitors (15 auxotrophs tested). We conclude that the polA1 mutation exerts a powerful mutator activity in this specific genetic context.
我们检测了在大肠杆菌K-12的polA1菌株过夜培养物中以大约10⁻³的频率积累的122个自发组氨酸营养缺陷型。其中113个似乎是负移码突变,9个似乎是缺失突变。在移码突变中,109个影响hisC基因,4个影响hisD、hisH、hisA和hisI基因。碱基替换的缺乏支持了聚合酶缺陷型polA是一种负移码和缺失型诱变剂的观点。与之前的报道相反,我们没有观察到PolA营养缺陷型比其原养型亲本生长更好(测试了15个营养缺陷型)。我们得出结论,在这种特定的遗传背景下,polA1突变发挥了强大的诱变活性。