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1
The timing of UV mutagenesis in yeast: a pedigree analysis of induced recessive mutation.酵母中紫外线诱变的时间:诱导隐性突变的谱系分析。
Genetics. 1977 Oct;87(2):237-48. doi: 10.1093/genetics/87.2.237.
2
The mutagenic potential of unexcised pyrimidine dimers in Saccharomyces cerevisiae, rad1-1: evidence from photoreactivation and pedigree analysis.
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3
Inducible nucleotide excision repair (NER) of UV-induced cyclobutane pyrimidine dimers in the cell cycle of the budding yeast Saccharomyces cerevisiae: evidence that inducible NER is confined to the G1 phase of the mitotic cell cycle.在出芽酵母酿酒酵母的细胞周期中紫外线诱导的环丁烷嘧啶二聚体的可诱导核苷酸切除修复:有证据表明可诱导核苷酸切除修复局限于有丝分裂细胞周期的G1期。
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4
Photoreactivation implicates cyclobutane dimers as the major promutagenic UVB lesions in yeast.
Mutat Res. 1992 Jul;268(1):83-94. doi: 10.1016/0027-5107(92)90086-h.
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Analysis of lethal events induced by ultraviolet in a heterokaryon of Neurospora.
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6
Initiation of UV mutagenesis in Saccharomyces cerevisiae.酿酒酵母中紫外线诱变的起始
Nature. 1978 Aug 31;274(5674):888-91. doi: 10.1038/274889a0.
7
Analysis of gene- and strand-specific repair in the moderately UV-sensitive Saccharomyces cerevisiae rad23 mutant.中度紫外线敏感的酿酒酵母rad23突变体中基因和链特异性修复的分析。
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UV-induced lethal sectoring and pure mutant clones in yeast.紫外线诱导的酵母致死扇形化和纯合突变克隆
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Three additional genes involved in pyrimidine dimer removal in Saccharomyces cerevisiae: RAD7, RAD14 and MMS19.酿酒酵母中参与嘧啶二聚体去除的另外三个基因:RAD7、RAD14和MMS19。
Mol Gen Genet. 1979 Nov;176(3):351-9. doi: 10.1007/BF00333097.

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Processing closely spaced lesions during Nucleotide Excision Repair triggers mutagenesis in E. coli.在核苷酸切除修复过程中处理紧密间隔的损伤会引发大肠杆菌中的诱变。
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DNA repair mechanisms and the bypass of DNA damage in Saccharomyces cerevisiae.酵母中 DNA 修复机制和 DNA 损伤的绕过。
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The mechanism of nucleotide excision repair-mediated UV-induced mutagenesis in nonproliferating cells.核苷酸切除修复介导的非增殖细胞中 UV 诱导突变的机制。
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High-resolution genome-wide analysis of irradiated (UV and γ-rays) diploid yeast cells reveals a high frequency of genomic loss of heterozygosity (LOH) events.高分辨率全基因组分析辐照(UV 和 γ 射线)二倍体酵母细胞揭示了高频的基因组杂合性丢失(LOH)事件。
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Random UV-C mutagenesis of Scheffersomyces (formerly Pichia) stipitis NRRL Y-7124 to improve anaerobic growth on lignocellulosic sugars.用随机紫外线诱变酿酒酵母(原毕赤酵母)NRRL Y-7124 以提高其在木质纤维素糖上的厌氧生长能力。
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The Saccharomyces cerevisiae RAD9, RAD17, RAD24 and MEC3 genes are required for tolerating irreparable, ultraviolet-induced DNA damage.酿酒酵母的RAD9、RAD17、RAD24和MEC3基因是耐受不可修复的紫外线诱导的DNA损伤所必需的。
Genetics. 1998 Sep;150(1):75-93. doi: 10.1093/genetics/150.1.75.
10
Efficient UV stimulation of yeast integrative transformation requires damage on both plasmid strands.对酵母整合转化进行高效紫外线刺激需要质粒两条链都受损。
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本文引用的文献

1
The repair hypothesis and the effect of caffeine on the induction of complete mutants in yeast.修复假说以及咖啡因对酵母中完全突变体诱导的影响。
Mutat Res. 1976 Jun;35(2):337-40. doi: 10.1016/0027-5107(76)90198-6.
2
UV-induced lethal sectoring and pure mutant clones in yeast.紫外线诱导的酵母致死扇形化和纯合突变克隆
Mutat Res. 1976 Aug;36(2):171-6. doi: 10.1016/0027-5107(76)90005-1.
3
Induction of pure and sectored mutant clones in excision-proficient and deficient strains of yeast.在酵母切除修复功能正常和缺陷的菌株中诱导纯合和扇形突变克隆。
Mutat Res. 1977 Jun;43(3):327-38. doi: 10.1016/0027-5107(77)90056-2.

酵母中紫外线诱变的时间:诱导隐性突变的谱系分析。

The timing of UV mutagenesis in yeast: a pedigree analysis of induced recessive mutation.

作者信息

James A P, Kilbey B J

出版信息

Genetics. 1977 Oct;87(2):237-48. doi: 10.1093/genetics/87.2.237.

DOI:10.1093/genetics/87.2.237
PMID:336459
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1213737/
Abstract

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.

摘要

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。