Loewen P C, Triggs B L, George C S, Hrabarchuk B E
J Bacteriol. 1985 May;162(2):661-7. doi: 10.1128/jb.162.2.661-667.1985.
A locus unlinked to either katE or katF that affected catalase levels in Escherichia coli was identified and localized between metB and ppc at 89.2 min on the genome. The locus was named katG. Mutations in katG which prevented the formation of both isoenzyme forms of the bifunctional catalase-peroxidase HPI were created both by nitrosoguanidine and by transposon Tn10 insertions. All katG+ recombinants and transductants contained both HPI isoenzymes. Despite the common feature of little or no catalase activity in four of the catalase-deficient strains, subtle differences in the phenotypes of each strain resulted from the different katG mutations. All three mutants caused by nitrosoguanidine produced a protein with little or no catalase activity but with the same subunit molecular weight and with similar antigenic properties to HPI, implying the presence of missense mutations rather than nonsense mutations in each strain. Indeed one mutant produced an HPI-like protein that retained peroxidase activity, whereas the HPI-like protein in a second mutant exhibited no catalase or peroxidase activity. The third mutant responded to ascorbate induction with the synthesis of near normal catalase levels, suggesting a regulatory defect. The Tn10 insertion mutant produced no catalase and no protein that was antigenically similar to HPI.
在大肠杆菌中,一个与katE或katF均不连锁、影响过氧化氢酶水平的基因座被鉴定出来,并定位在基因组89.2分钟处的metB和ppc之间。该基因座被命名为katG。通过亚硝基胍和转座子Tn10插入,均产生了katG突变,这些突变阻止了双功能过氧化氢酶-过氧化物酶HPI两种同工酶形式的形成。所有katG+重组体和转导子均含有两种HPI同工酶。尽管四个过氧化氢酶缺陷菌株都有共同的特征,即过氧化氢酶活性很低或没有,但每个菌株表型的细微差异是由不同的katG突变导致的。由亚硝基胍引起的所有三个突变体都产生了一种蛋白质,其过氧化氢酶活性很低或没有,但亚基分子量相同,且与HPI具有相似的抗原特性,这意味着每个菌株中存在错义突变而非无义突变。实际上,一个突变体产生了一种保留过氧化物酶活性的HPI样蛋白,而第二个突变体中的HPI样蛋白既没有过氧化氢酶活性也没有过氧化物酶活性。第三个突变体在抗坏血酸诱导下,合成的过氧化氢酶水平接近正常,表明存在调控缺陷。Tn10插入突变体不产生过氧化氢酶,也不产生与HPI抗原相似的蛋白质。