Maurer R, Wong A
Department of Molecular Biology and Microbiology, Case Western Reserve University, Cleveland, Ohio 44106.
J Bacteriol. 1988 Aug;170(8):3682-8. doi: 10.1128/jb.170.8.3682-3688.1988.
A class of dominant lethal mutations in the dnaB (replicative helicase) gene of Salmonella typhimurium is described. The mutated genes, when present on multicopy plasmids, interfered with colony formation by Escherichia coli host strains with a functional chromosomal dnaB gene. The lethal phenotype was expressed specifically in supE (glutamine-inserting) host strains and not in Sup+ strains, because the mutant genes, by design, also possessed an amber mutation derived from a glutamine codon. Mutations located at 11 sites by deletion mapping and DNA sequence analysis varied in the temperature dependence and severity of their lethal effects. None of the mutations complemented a dnaB(Ts) host strain at high temperature (42 degrees C). Therefore, these nonfunctional DnaB proteins must engage some component(s) of the DNA replication machinery and inhibit replication. These mutations are predicted to confer limited, specific defects in either the catalytic activity of DnaB or the ability of DnaB to interact with one of its ligands such as DNA, nucleotide, or another replication protein. The variety of mutant sites and detailed phenotypes represented in this group of mutations may indicate the operation of more than one specific mechanism of lethality.
描述了鼠伤寒沙门氏菌dnaB(复制解旋酶)基因中的一类显性致死突变。当突变基因存在于多拷贝质粒上时,会干扰具有功能性染色体dnaB基因的大肠杆菌宿主菌株的菌落形成。致死表型在supE(谷氨酰胺插入)宿主菌株中特异性表达,而在Sup+菌株中不表达,因为突变基因经设计还具有源自谷氨酰胺密码子的琥珀突变。通过缺失定位和DNA序列分析确定位于11个位点的突变在致死效应的温度依赖性和严重程度上有所不同。在高温(42℃)下,没有一个突变能互补dnaB(Ts)宿主菌株。因此,这些无功能的DnaB蛋白必定与DNA复制机制的某些成分相互作用并抑制复制。预计这些突变会在DnaB的催化活性或DnaB与诸如DNA、核苷酸或另一种复制蛋白等配体之一相互作用的能力方面产生有限的、特定的缺陷。这组突变中所呈现的各种突变位点和详细表型可能表明存在不止一种特定的致死机制。