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粗糙脉孢菌中的修复抗性突变

Repair-resistant mutation in Neurospora.

作者信息

Stadler D, Macleod H, Loo M

出版信息

Genetics. 1987 Jun;116(2):207-14. doi: 10.1093/genetics/116.2.207.

Abstract

Chronic UV treatment produces severalfold fewer mutations in Neurospora conidia than does the same total dose of acute UV. Experiments were designed to determine the conditions required for chronic UV mutagenesis. Measurement of the coincidence frequency for two independent mutations revealed the existence of a subset of cells which are mutable by chronic UV. Analysis of forward mutation at the mtr locus showed that the genetic alterations produced by chronic UV were virtually all point mutants, even though the assay system could detect alterations or deletions extending into neighboring genes. A significant fraction of the mutants produced by acute UV were multigenic deletions. The size of the dose-rate effect (acute UV mutation frequency divided by chronic UV mutation frequency) was compared for several different mutation assay systems. Forward mutations (recessive lethals and mtr) gave values ranging from four to nine. For events which were restricted to specific molecular sites (specific reversions and nonsense suppressor mutations), there was a wider range of dose-rate ratios. This suggests that chronic UV mutation may be restricted to certain molecular sequences or configurations.

摘要

与相同总剂量的急性紫外线相比,慢性紫外线处理在粗糙脉孢菌分生孢子中产生的突变要少几倍。设计实验以确定慢性紫外线诱变所需的条件。对两个独立突变的并发频率进行测量,揭示了存在一部分可被慢性紫外线诱变的细胞。对mtr位点正向突变的分析表明,即使检测系统能够检测到延伸至相邻基因的改变或缺失,慢性紫外线产生的遗传改变实际上几乎都是点突变。急性紫外线产生的很大一部分突变体是多基因缺失。比较了几种不同突变检测系统的剂量率效应大小(急性紫外线突变频率除以慢性紫外线突变频率)。正向突变(隐性致死突变和mtr突变)给出的值范围为4至9。对于限于特定分子位点的事件(特定回复突变和无义抑制突变),剂量率比值范围更广。这表明慢性紫外线突变可能限于某些分子序列或构型。

相似文献

1
Repair-resistant mutation in Neurospora.粗糙脉孢菌中的修复抗性突变
Genetics. 1987 Jun;116(2):207-14. doi: 10.1093/genetics/116.2.207.
2
A dose-rate effect in UV mutagenesis in neurospora.
Mutat Res. 1984 Jun;127(1):39-47. doi: 10.1016/0027-5107(84)90138-6.
3
Analysis of lethal events induced by ultraviolet in a heterokaryon of Neurospora.
Mol Gen Genet. 1979 Mar 9;171(1):59-68. doi: 10.1007/BF00274015.

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