Ionizing and Ultraviolet Radiations: Genetic Effects and Repair in Yeast

Moustacchi, E.; Chanet, Roland; Heude, M.

doi:10.1007/978-1-4613-4160-4_21

Cited by 7 publications

(1 citation statement)

References 62 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There now exists a considerable body of information on repair and mutagsnesis in Saccharomyces cerevisiae. Although certain aspects of this subject have been reviewed in the past [19,56,121,164], the present summary will attempt to broaden our current understanding not only by including more recent genetic data, but also by emphasizing the interrelation betwaen cellular processes that involve DMA metabolism, namely repair, mutagenesis, recombination and replication; also included are developmental systems regulating the sexual cycle which affect chromatin indirectly.…”

mentioning

confidence: 99%

Genetic and physiological factors affecting repair and mutagenesis in yeast

Lemontt¹

1979

View full text Add to dashboard Cite

Current views of DNA repair and mutagenesis in the yeast Saccharomyces cerevisiae are discussed in the light of recent data, and with emphasis on the isolation and characterization of genetically well-defined mutations that affect DNA metabolism in general (including replication and recombination). Various "pathways" of repair are described particularly in relation to their involvement in mutagenic mechanisms. In addition to genetic control, certain physiological factors such as "cell age", DNA replication and the regulatory state of the mating-type locus, are shown to also play a role in repair and mutagenesis.

show abstract

mentioning

confidence: 99%

Genetic and physiological factors affecting repair and mutagenesis in yeast

Lemontt¹

1979

View full text Add to dashboard Cite

show abstract

Nalidixic acid inhibition of post‐ultraviolet recovery by nalidixic acid sensitive and resistant strains of Candida albicans

Sarachek

Lee

1980

J of Basic Microbiology

View full text Add to dashboard Cite

Nalidixic acid (Nal) can kill Candida albicans directly or suppress the organism's recovery from ultraviolet irradiation. Nutants selected for resistance to inactivation by Nal alone have generally enhanced DNA repair proficiencies evidenced by their coincident increased resistances to ultraviolet radiation, ethylmethane sulfonate, and nitrous acid. The effects of Nal, erythromycin, and inhibitors of oxidative phosphorylation on survivals of mutant and wild type strains following ultraviolet exposure indicate that different mechanisms underly the direct lethality of Nal and its ability to inhibit post-irradiation recovery.The bacteriocidal agent, nalidixic acid (Nal), selectively inhibits deoxyribonucleic acid (DNA) synthesis in procaryotes by interfering with the nicking-closing activity of the gyrase component of theDNA replication apparatus (SUGINO et al. 1977). During growth on inhibitory levels of Nal, cells accumulate single strand breaks in DNA and undergo inactivation a t proportionate rates ( HILL and FANGMAN 1973). The likelihood that DNA damage is the direct cause of death is supported by the observation that genetic defects at various points in either excision or recombination DNA repair systems accentuate cellular sensitivity to the drug (MCDANIEL et al. 1978). At concentrations far below the bacteriocidal level, Nal will decrease survival of ultraviolet (UV) irradiated Escherichia coli, but only in strains carrying functional rec BC genes (PURDY and YIELDING 1976). The rec B and rec C loci specify separate subunits of the adenosine 5'-triphosphate dependent deoxyribonuclease, exonuclease V, required for recombination repair of DNA. Though requirement for rec BC product indicates that the post-UVeffect of low levels of Nal probably is due to interference with enzymatic repair of DNA, the effect cannot be ascribed simply to inhibition by Nal of exonuclease V activity: appreciable exonucleaae V activity must occur even in the presence of much higher concentrations of the drug since the bacteriocidal action of N a l alone increases greatly when the enzyme's activity is reduced by mutation at either rec B or C (MCDANIEL et al. 1978). But whatever the underlying mechanisms, Nal evidently can kill bacteria either through direct damage to DNA or by impeding repair of DNA damage caused by other agents.In eucaryotic n~icroorganisms, Na 1 selectively inhibits synthesis of the procaryote-

show abstract

Nalidixic acid inhibition of post-ultraviolet recovery by nalidixic acid sensitive and resistant strains ofCandida albicans

Sarachek¹,

Lee²

1980

Z Allg Mikrobiol

View full text Add to dashboard Cite

Nalidixic acid (Nal) can kill Candida albicans directly or suppress the organism's recovery from ultraviolet irradiation. Mutants selected for resistance to inactivation by Nal alone have generally enhanced DNA repair proficiencies evidenced by their coincident increased resistances to ultraviolet radiation, ethylmethane sulfonate, and nitrous acid. The effects of Nal, erythromycin, and inhibitors of oxidative phosphorylation on survivals of mutant and wild type strains following ultraviolet exposure indicate that different mechanisms underly the direct lethality of Nal and its ability to inhibit post-irradiation recovery.

show abstract

Ionizing and Ultraviolet Radiations: Genetic Effects and Repair in Yeast

Cited by 7 publications

References 62 publications

Genetic and physiological factors affecting repair and mutagenesis in yeast

Genetic and physiological factors affecting repair and mutagenesis in yeast

Nalidixic acid inhibition of post‐ultraviolet recovery by nalidixic acid sensitive and resistant strains of Candida albicans

Nalidixic acid inhibition of post-ultraviolet recovery by nalidixic acid sensitive and resistant strains ofCandida albicans

Contact Info

Product

Resources

About