Yarosh D B
J Virol. 1978 May;26(2):265-71. doi: 10.1128/JVI.26.2.265-271.1978.
Two late gene am mutants of bacteriophage T4 that can be induced to revert by UV were crossed to a temperature-sensitive ligase mutant. In the double mutants, UV-induced reversion was eliminated at a semirestrictive temperature. When the single am mutants were irradiated and then allowed a single passage in a permissive host, the UV-induced reversion frequency was increased by 15- to 25-fold. This increased mutagenesis was also abolished by the presence of the ligase allele. When the UV-irradiated single am mutants multiply infected a permissive host, allowing multiplicity reactivation to occur, the induced reversion frequency was reduced similarly to the reduction in lethality. The mutagenesis that remained was again abolished by the presence of the ligase allele. It is concluded that UV induces mutations in phage T4 through the action of a pathway that includes polynucleotide ligase. The increase in mutation frequency after growth in a permissive host implies that mutagenesis can occur at more than one stage of the infection rather than only in an early stage before expression of the mutant genome. The process of multiplicity reactivation appears to be error-free since it overcomes lethal lesions without inducing new mutations.
两个可被紫外线诱导回复突变的噬菌体T4晚期基因am突变体与一个温度敏感的连接酶突变体进行了杂交。在双突变体中,紫外线诱导的回复突变在半限制温度下被消除。当单个am突变体受到紫外线照射,然后在允许宿主中传代一次时,紫外线诱导的回复突变频率增加了15至25倍。这种增加的诱变作用也因连接酶等位基因的存在而被消除。当紫外线照射的单个am突变体多重感染允许宿主,从而发生多重复活时,诱导的回复突变频率也类似地降低,与致死率的降低情况相同。剩余的诱变作用再次因连接酶等位基因的存在而被消除。得出的结论是,紫外线通过包括多核苷酸连接酶的一条途径的作用在噬菌体T4中诱导突变。在允许宿主中生长后突变频率的增加意味着诱变可以在感染的多个阶段发生,而不仅仅是在突变基因组表达之前的早期阶段。多重复活过程似乎是无差错的,因为它克服了致死性损伤而不诱导新的突变。