Quiñones A, Piechocki R
Wissenschaftsbereich Genetik, Martin-Luther-Universität Halle-Wittenberg, DDR-Halle/Saale.
J Basic Microbiol. 1987;27(5):263-73. doi: 10.1002/jobm.3620270508.
We have constructed double mutants carrying either ssb-1 or ssb-113 alleles, which encode temperature-sensitive single strand DNA binding proteins (SSB), and the uvrD::Tn5 allele causing deficiency in DNA helicase II, and have examined sensitivity to ultraviolet light (UV), recombination and spontaneous as well as UV-induced mutagenesis. We have found in a recA+ background that (i) none of the ssb uvrD double mutants was more sensitive to UV than either single mutant; (ii) the ssb-1 allele partially suppressed the strong UV sensitivity of uvrD::Tn5 mutants; (iii) in the recA730 background with constitutive SOS expression, the ssb-1 and ssb-113 alleles suppressed the strong UV-sensitivity caused by the uvrD::Tn5 mutation; (iv) in ssb-113 mutants, the level of recombination was reduced only 10-fold but 100-fold in ssb-1 mutants, showing that there was no correlation between the DNA repair deficiency and the recombination deficiency; (v) the hyper-recombination phenotype of the uvrD::Tn5 mutant was suppressed by the addition of either the ssb-1 or the ssb-113 allele; (vi) no addition of the spontaneous mutator effects promoted by the uvrD::Tn5 and the ssb-113 alleles was observed. These results suggest a possible functional interaction between SSB and Helicase II in DNA repair and mutagenesis.
我们构建了携带ssb - 1或ssb - 113等位基因(编码温度敏感型单链DNA结合蛋白(SSB))以及uvrD::Tn5等位基因(导致DNA解旋酶II缺陷)的双突变体,并检测了它们对紫外线(UV)的敏感性、重组情况以及自发和UV诱导的诱变。我们发现在recA+背景下:(i)没有一个ssb uvrD双突变体对UV的敏感性比任何一个单突变体更高;(ii)ssb - 1等位基因部分抑制了uvrD::Tn5突变体对UV的强敏感性;(iii)在具有组成型SOS表达的recA730背景下,ssb - 1和ssb - 113等位基因抑制了由uvrD::Tn5突变引起的对UV的强敏感性;(iv)在ssb - 113突变体中,重组水平仅降低了10倍,而在ssb - 1突变体中降低了100倍,表明DNA修复缺陷与重组缺陷之间没有相关性;(v)uvrD::Tn5突变体的高重组表型被添加的ssb - 1或ssb - 113等位基因所抑制;(vi)未观察到uvrD::Tn5和ssb - 113等位基因促进的自发诱变效应。这些结果表明在DNA修复和诱变过程中,SSB和解旋酶II之间可能存在功能相互作用。