A dose-rate effect in UV mutagenesis in Neurospora

Stadler, David; Macleod, Helen

doi:10.1016/0027-5107(84)90138-6

Cited by 7 publications

(4 citation statements)

References 11 publications

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“…Double-strand breaks (RESNICK and MARTIN 1976) and deletion mutations (DESERRES, MALLINC and WEBBER 1967) are both characteristics of X-ray mutagenesis and may be correlated in a repair pathway. The occurrence of such pairs of dimers should display two-hit kinetics; such induction curves have been reported for mutagenesis by acute UV in Neurospora (DESERRES and KILBEY 1971;STADLER and MACLEOD 1984). Chronic UV would seldom produce pairs of neighboring dimers at the same time, so double-strand breaks might be avoided.…”

Section: Discussionmentioning

confidence: 83%

“…As pointed out above, the mutations which occur after chronic UV treatment are of special interest because they may represent repair-resistant mutations: those which occur after a limited mutagenic challenge to cells with functioning repair systems operating in ideal physiological conditions. These conditions were met in the earlier study of recessive lethal mutations (STADLER and MACLEOD 1984), as the cells were incubated in optimal growth medium during the days following the UV treatment (before being assayed for mutations). The experiments reported here involved a limitation which should be noted.…”

Section: Discussionmentioning

confidence: 99%

“…T h e heterokaryon was grown on minimal medium plus anthranilate. Conidia were suspended in water at 22" and treated with 5000 erg/mmz of chronic or acute UV as described earlier (STADLER and MACLEOD 1984). The duration of treatment was 2 min for acute UV and 310 min for chronic UV.…”

Section: Methodsmentioning

confidence: 99%

“…Treated conidia were diluted and plated on minimal medium plus anthranilate (Anth) at such a concentration as to produce about 50 heterokaryotic colonies per plate from the surviving conidia. These plates were replicated to medium supplemented with anthranilate plus lysine plus fluorophenylalanine (ALF) and to anthranilate plus adenine plus cycloheximide (ADC) to detect recessive lethal mutation in one or the other of the homokaryon components, as described by STADLER and MACLEOD (1984) and shown in Figure 1. T h e basic principle of the test concerns the fact that a heterokaryotic conidium grows into a colony which produces abundant conidia of all three genetic types; heterokaryons and the two classes of homokaryons.…”

Section: Methodsmentioning

confidence: 99%

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Repair-Resistant Mutation in Neurospora

1987

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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.

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Repair-Resistant Mutation in Neurospora

1987

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Genetics of Neurospora

Davis

1995

Genetics and Biotechnology

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Excision of pyrimidine dimers from the DNA of Neurospora

Macleod

Stadler

1986

Mol Gen Genet

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Germinated conidia of Neurospora have been monitored for their ability to excise pyrimidine dimers. Dimer concentration was measured in DNA extracted immediately after UV treatment, and it was compared to that of DNA from cells which had a post-UV incubation before extraction. Two methods were used to assay dimer level in DNA: measurement of the number of single-strand breaks (as revealed in alkaline sucrose gradients) produced by a dimer-specific endonuclease; monitoring the ability to compete for binding to dimer-specific antibodies in a radioimmunoassay. Both methods showed efficient excision of dimers by wild-type and by uvs-2, even though an earlier study had reported that uvs-2 was unable to excise dimers. UV-induced mutation shows a dose-rate effect: acute UV yields several times as many mutations as does the same dose of chronic UV. There is a parallel effect on dimer accumulation. The concentration of dimers at the conclusion of the UV treatment shows a strong correlation with the resultant mutation frequency.

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A dose-rate effect in UV mutagenesis in Neurospora

Cited by 7 publications

References 11 publications

Repair-Resistant Mutation in Neurospora

Repair-Resistant Mutation in Neurospora

Genetics of Neurospora

Excision of pyrimidine dimers from the DNA of Neurospora

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