Bass I A, Gorlenko Zh M, Danilevskaia O N, Dmitriev A D, Kaliaeva E S
Mol Biol (Mosk). 1978 Jan-Feb;12(1):191-205.
In merodiploid cells containing a double dose of structural genes of RNA polymerase subunits--rpoB and rpoC--the rate of synthesis of beta- and beta'-subunits is 2 times higher than in haploid cells. Missense mutation rpoC1 (tsX) in the beta'-polypeptide gene accelerates the synthesis of both beta- and beta'-subunits, particularly at a nonpermissive temperature. When rpoB-rpoC operon containing mutation rpoC1 is duplicated no dose effect of these genes is observed. In the heterozygous state mutation rpoC1 produces almost no accelerating effect on the synthesis of RNA polymerase subunits i. e. is recessive with respect to the wild allele of rpoC. In the presence of rifampicin the synthesis of RNA polymerase subunits in a sensitive wild-type strain is stimulated 6-fold, the same effect is observed with cells carrying mutation rpoC1, the latter, however, itself accelerates the synthesis of these subunits 3-fold. Thus the effects of rifampicin and the mutation are synergistic indicating that these factors act independently. Similar data have also been obtained with rifampicin-treated cells of rpoB22 amber-mutant. In UV-irradiated cells, amino acid incorporation into beta- and beta'-subunits declines more rapidly than into the total protein. When either irradiated or non-irradiated cells are infected with a transducing phage lambdarifd-47 which carries rpoB gene, the synthesis of beta-proceeds at a higher rate. Irradiation of bacteria before the infection (500 erg/mm2) results in 6.5-fold acceleration of the synthesis induced by subsequent infection with lambdarifd-47 as compared to non-infected non-irradiated cells; the fraction of newly formed beta-polypeptide with respect to total protein grows 20-fold in this case. The data are considered with regard to the possible mechanisms of regulation of synthesis of RNA polymerase subunits.
在含有双倍剂量RNA聚合酶亚基结构基因(rpoB和rpoC)的部分二倍体细胞中,β亚基和β'亚基的合成速率比单倍体细胞高2倍。β'多肽基因中的错义突变rpoC1(tsX)加速了β亚基和β'亚基的合成,尤其是在非允许温度下。当含有突变rpoC1的rpoB - rpoC操纵子被复制时,未观察到这些基因的剂量效应。在杂合状态下,突变rpoC1对RNA聚合酶亚基的合成几乎没有加速作用,即相对于rpoC的野生等位基因是隐性的。在利福平存在的情况下,敏感野生型菌株中RNA聚合酶亚基的合成被刺激6倍,携带突变rpoC1的细胞也观察到相同的效果,然而,后者本身使这些亚基的合成加速3倍。因此利福平和突变的作用是协同的,表明这些因素独立起作用。用利福平处理的rpoB22琥珀突变体细胞也获得了类似的数据。在紫外线照射的细胞中,氨基酸掺入β亚基和β'亚基的速度比掺入总蛋白的速度下降得更快。当用携带rpoB基因的转导噬菌体λrifd - 47感染照射过或未照射过的细胞时,β亚基的合成速率更高。感染前对细菌进行照射(500尔格/平方毫米)导致与未感染未照射细胞相比,随后用λrifd - 47感染诱导的合成加速6.5倍;在这种情况下,新形成的β多肽相对于总蛋白的比例增长20倍。关于RNA聚合酶亚基合成调控的可能机制对这些数据进行了讨论。