James A P, Kilbey B J
Genetics. 1977 Oct;87(2):237-48. doi: 10.1093/genetics/87.2.237.
The mechanism of UV-induced mutation in eukaryotes was studied in individual yeast cells by a procedure that combined pedigree analysis and tetrad analysis. The technique involved the induction of recessive lethals and semilethals in G1 diploid cells. Induced frequencies were 25 and 61 percent at survival levels of 90 and 77 percent, respectively. No evidence of gross chromosome aberrations was detected. Recessive mutations that affect only one strand or that affect both strands of the DNA molecule are induced much at random among a population of cells, and both types can occur within the same cell. However, the data confirm that two-strand mutations are in the majority after a low level of irradiation. The simplest explanation involves a mechanism whereby most mutations are fixed in both strands prior to the first round of post-irradiation DNA replication. The recessive mutational consequences of irradiation are exhausted at the conclusion of the first post-irradiation cell division, although dominant-lethal sectoring continues at a high level through the second post-irradiation division. It is concluded that pyrimidine dimers that persist to the second round of DNA replication are rare or ineffective.
通过结合谱系分析和四分体分析的方法,在单个酵母细胞中研究了真核生物紫外线诱导突变的机制。该技术涉及在G1二倍体细胞中诱导隐性致死突变和半致死突变。在存活率分别为90%和77%时,诱导频率分别为25%和61%。未检测到明显染色体畸变的证据。在一群细胞中,仅影响一条链或同时影响DNA分子两条链的隐性突变是随机诱导产生的,且两种类型都可在同一细胞内发生。然而,数据证实低剂量照射后双链突变占多数。最简单的解释涉及一种机制,即大多数突变在第一轮照射后DNA复制之前就已在两条链上固定。照射的隐性突变后果在照射后第一次细胞分裂结束时就已耗尽,尽管显性致死性扇形化在照射后第二次分裂期间仍处于高水平。得出的结论是,持续到第二轮DNA复制的嘧啶二聚体很少或没有作用。