Dear Kris,
> The title is
> UV mutagenesis of yeast: A comparative study of the repair processes. I am
> having a very hard time finding relevant literature and information about
> yeast, UV mutagenesis of yeast, the repair processes photoreactive and dark
> repair, and the strain Saccharomyces cerevisiae.
We have a program we produce here at GenBank/NCBI which allows you to
search a subset of the Medline database, and we have a beta (testing)
version which allows you to take a paragraph to search the 'neighbors'
(related articles) ... So I used the above paragraph, and obtained 30
references. I append these, with their abstract, below. You will find
some of thme quite relevent (and others less!). You may want to look
them up at a University library near you. This does look pretty
advanced for a science project, so I imagine you are a senior ;-)
If you have a real Internet connection (via a SLIP or PPP if you use a
modem) you can get Network Entrez which is a compilation of all known
DNA sequences, all known protein sequences, and a subset of Medline
references and abstracts (the current version has about 1.2 million out
of the 4-5 million which encompass all of Medline).
Medline is about 4-5000 medicaly oriented journal which are scanned and
anotated in an electronic format, and made available in various way,
through various distributors. We (at GenBank) make a subset available
through the Internet and CD-ROMs. The CD-ROM subset is even smaller,
only 200,000 records.
Hope this helps,
francis
--
| B.F. Francis Ouellette | tel: (301) 496-2475 |
| GenBank | fax: (301) 480-9241 |
| | NCBI/NLM/NIH Building 38A |
|francis at ncbi.nlm.nih.gov | Bethesda, MD 20894, USA |
J Basic Microbiol 29: 675-83 (1989) [90218669]
Auxotrophic mutants of the yeast Trichosporon adeninovorans.
I. A. Samsonova, F. Bottcher, C. Werner & R. Bode
Ernst-Moritz-Arndt-Universitat Greifswald, Sektion Biologie.
We have isolated and characterized auxotrophic mutants of Trichosporon
adeninovorans, strain PAR-4 to get genetic markers that cover the entire
nuclear genome of this thermotolerant yeast of technological interest. The
nitrosoguanidine mutagenesis yielded mutants at a high frequency. We detected a
broad spectrum of auxotrophic phenotypes in the random mutant samples.
Obviously, strain PAR-4 is a haploid or hyperhaploid yeast. In correspondence
we determined a low DNA content per cell. In contrast to NG1), UV light was an
inefficient mutagen. UV survival curves were without the typical shoulder
indicating suppression of repair of UV-induced lethal lesions. Thus, the
response of PAR-4 to UV was different from those of Saccharomyces cerevisiae
and other yeasts.
MeSH Terms:
Dose-Response Relationship, Radiation
*Genetic Markers
Genotype
Haploidy
Hyphomycetes/*genetics
*Mutation
Phenotype
Trichosporon/*genetics/radiation effects
Ultraviolet Rays
Substances:
Genetic Markers
Curr Genet 21: 93-4 (1992) [92233494]
Repair of ultraviolet light damage in Saccharomyces cerevisiae as studied with
double- and single-stranded incoming DNAs.
D. Keszenman-Pereyra & K. Hieda
Department of Physics, Rikkyo University, Tokyo, Japan.
Purified double- and single-stranded DNAs of the autonomously replicating
vector M13RK9-T were irradiated with ultraviolet light (UV) in vitro and
introduced into competent whole cells of Saccharomyces cerevisiae. Incoming
double-stranded DNA was more sensitive to UV in excision repair-deficient rad2-
1 cells than in proficient repair RAD+ cells, while single-stranded DNA
exhibited high sensitivity in both host cells. The results indicate that in
yeast there is no effective rescue of UV-incoming single-stranded DNA by
excision repair or other constitutive dark repair processes.
MeSH Terms:
DNA Damage
*DNA Repair
DNA, Fungal/radiation effects
DNA, Single-Stranded/radiation effects
Saccharomyces cerevisiae/*genetics/growth & development/radiation effects
Ultraviolet Rays
Substances:
DNA, Fungal
DNA, Single-Stranded
Mutat Res 60: 163-71 (1979) [79221677]
The mutagenic potential of unexcised pyrimidine dimers in Saccharomyces
cerevisiae, rad1-1: evidence from photoreactivation and pedigree analysis.
B. J. Kilbey & A. P. James
Photoreactivation and pedigree analysis have been combined to show that
unexcised pyrimidine dimers in the DNA of rad1-1 yeast can initiate
mutagenesis after passing through several DNA replications. Monomerisation of
dimers immediately before the second replication to follow UV has no effect on
mutants appearing after the first post-UV cell division but reduces second-
generation mutants to one third of their frequency in the dark and has a
similar through slightly less marked effect on mutants appearing in the third
or subsequent generations. The bearing of these findings on the mechanism of UV
mutagenesis is dicussed.
MeSH Terms:
DNA/radiation effects
DNA Replication
*Mutagens
Mutation
Pyrimidine Dimers/*pharmacology
Saccharomyces cerevisiae/*genetics
Ultraviolet Rays
Mutat Res 289: 55-60 (1993) [93361032]
Cellular recovery, DNA repair and mutagenesis--a tale of two yeasts.
A. Nasim & M. A. Hannan
Department of Biological and Medical Research, King Faisal Specialist Hospital
and Research Centre, Riyadh, Saudi Arabia.
In studies related to recovery and repair mechanisms following DNA damage, one
problem that has been frequently addressed concerns the effects of DNA repair
on both spontaneous and induced mutagenesis. Among the eukaryotic organisms
which served as unique and valuable systems for investigating this problem are
the two yeasts, Saccharomyces cerevisiae and Schizosaccharomyces pombe. With
the basic genetics well worked out in both, these yeasts have provided the
experimental tools for comparative analysis of mechanisms of DNA repair which
show a great deal of diversity between the two unicellular eukaryotes. Since
the present issue focuses on the contributions of R.H. Haynes to the area of
DNA repair and mutagenesis, we have chosen to discuss those specific aspects of
our studies which are directly or indirectly related to or influenced by his
research in this field. These include: (i) liquid holding recovery, (ii)
production of two strand mutations and the concept of heteroduplex repair, and
(iii) understanding of pathways of repair through construction of
supersensitive mutants in yeast.
MeSH Terms:
*DNA Repair
*Mutagenesis
Mutation
Saccharomyces cerevisiae/*genetics
Schizosaccharomyces/*genetics
Mol Gen Genet 190: 406-12 (1983) [83270763]
Analysis of mutagenic DNA repair in a thermoconditional repair mutant of
Saccharomyces cerevisiae. I. Influence of cycloheximide on UV-irradiated
stationary phase rev2ts cells.
W. Siede, F. Eckardt & M. Brendel
Using the thermoconditional yeast mutant rev2ts that controls an apparently
site-specific step of mutagenic DNA repair it was possible to measure the time
course of REV2 dependent UV-induced reversion of the ochre allele his5-2 and
recovery of survival for UV-treated stationary phase cells: due to the rev2ts
coded protein being active at 23 degrees C, survival and mutation frequencies
increased with duration of incubation under permissive conditions in growth
medium before the temperature was shifted to 36 degrees C (restrictive
temperature). This increase was abolished in the presence of the protein
synthesis inhibitor, cycloheximide. Furthermore, the REV2 dependent recovery of
survival could be blocked or nearly blocked by cycloheximide added at any time
during repair. Therefore, REV2 dependent repair can be characterized as a
process requiring concomitant protein synthesis. These findings give further
support to the concept that in yeast, mutagenesis involves UV inducible
components of DNA repair.
MeSH Terms:
Cycloheximide/pharmacology
*DNA Repair/drug effects
Fungal Proteins/biosynthesis
*Mutation
Saccharomyces cerevisiae/*genetics/radiation effects
Support, Non-U.S. Gov't
Temperature
Ultraviolet Rays
Substances:
Cycloheximide (CAS 66-81-9)
Fungal Proteins
Mol Gen Genet 221: 353-7 (1990) [90340285]
Repair of alkylation damage in Saccharomyces cerevisiae.
R. Goth-Goldstein & P. L. Johnson
Cell and Molecular Biology Division, Lawrence Berkeley Laboratory, Berkeley, CA
94720.
Repair of methylated bases in Saccharomyces cerevisiae was measured by two
methods: in vitro in cell extracts, and in vivo, by determining the loss of
methylated bases from yeast DNA after treatment of stationary cultures with
[3H]-N-methyl-N'-nitro-N-nitrosoguanidine. Whereas no repair activity could be
detected by the in vitro method, the methylated bases were removed in vivo very
efficiently. These contradictory results of in vitro and in vivo repair
measurements suggest that either the repair enzymes of yeast are sufficiently
different from those of bacteria and mammalian cells that they are not active
in the in vitro assay, or that methylated bases are repaired in yeast by a
different pathway.
MeSH Terms:
Alkylation
*DNA Damage
*DNA Repair
DNA, Fungal/*drug effects
Nitrosamines/*pharmacology
Saccharomyces cerevisiae/drug effects/*genetics
Support, U.S. Gov't, Non-P.H.S.
Support, U.S. Gov't, P.H.S.
Substances:
DNA, Fungal
Nitrosamines
3-(methylnitrosamino)propionitrile (CAS 60153-49-3)
Mutat Res 50: 181-93 (1978) [78176997]
Biochemical analysis of damage induced in yeast by formaldehyde. I. Induction
of single-strand breaks in DNA and their repair.
N. Magana-Schwencke, B. Ekert & E. Moustacchi
Analysis of sedimentation profiles in alkaline sucrose gradients showed that,
through a metabolic process, formaldehyde (FA) produced single-strand breaks in
DNA of exponential phase cells of haploid wild-type Saccharomyces cerevisiae.
The production of this type of lesion was dose-dependent. Strains defective in
excision-repair of pyrimidine dimers induced by ultraviolet (UV) irradiation
showed a reduced capacity to undergo single-stand breaks after treatment with
FA. This indicates that the repair pathways of damage induced by UV and FA
share a common step. Post-treatment incubation of wild-type cells in growth
medium indicate a lag in cell division during which a slow recovery of DNA with
a normal size was observed.
MeSH Terms:
DNA/*metabolism
*DNA Repair
Dose-Response Relationship, Drug
Formaldehyde/*pharmacology
Molecular Weight
*Mutagens
Saccharomyces cerevisiae
Genetics 82: 207-32 (1976) [76165998]
UV mutagenesis in radiation-sensitive strains of yeast.
C. W. Lawrence & R. Christensen
The yeast Saccharomyces cerevisiae appears to possess a single mutagenic or
"error prony" pathway for the repair of UV damage; rev1, rev2, rev3 (Lemontt
1971a), rad6, rad8, rad9 and rad18 (Lawrence et al. 1974; present results).
Strains carrying rad6 are the most sensitive to the lethal effects of UV light
in this group and double mutants carrying rad6 and either rev1, rev3, rad9 or
rad18 are no more sensitive than this single mutant strain, rev3 rad6 doubl-
mutant diploids failed to show any UV-induced reversion of the normally highly
reversion of the normally highly revertible ochre allele cycl-9, even though a
total of more than 2.5 X 10(9) viable cells was examined, suggesting that
strains of this kind are entirely UV-immutable; spontaneous revertants could be
recovered, however.-The rad6 and rev3 gene products would appear to be
necessary for all kinds of mutagenic events at all sites within the genome, but
the products of the other genes that act in the "error-prone" pathway have a
more restricted role and are involved in the production of only some kinds of
mutations. It is suggested that such selectivity arises from the interaction of
some repair enzymes with specific nucleotide sequences.
MeSH Terms:
*DNA Repair
Diploidy
Dose-Response Relationship, Radiation
Gene Frequency
Genes
Genotype
*Mutation
Phenotype
Radiation Genetics
Saccharomyces cerevisiae/*radiation effects
Support, U.S. Gov't, P.H.S.
*Ultraviolet Rays
Basic Life Sci 15: 85-120 (1980) [81159926]
Genetic and physiological factors affecting repair and mutagenesis in yeast.
J. F. Lemontt
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.
MeSH Terms:
*DNA Repair
DNA Replication
DNA, Fungal/metabolism
Mutagens/pharmacology
*Mutation
Ploidies
Radiation, Ionizing
Recombination, Genetic
Saccharomyces cerevisiae/drug effects/*genetics/radiation effects
Support, U.S. Gov't, Non-P.H.S.
Ultraviolet Rays
Substances:
Mutagens
DNA, Fungal
Mol Gen Genet 195: 487-90 (1984) [84294899]
UV-induced reversion of his4 frameshift mutations in rad6, rev1, and rev3
mutants of yeast.
C. W. Lawrence, T. O'Brien & J. Bond
The UV-induced reversion of two his4 frameshift alleles was much reduced in
rad6 mutants of Saccharomyces cerevisiae, an observation that is consistent
with the hypothesis that RAD6 function is required for the induction of all
types of genetic alteration in misrepair mutagenesis. The reversion of these
his4 alleles, together with two others of the same type, was also reduced in
rev1 and rev3 mutant strains; in these, however, the extent of the reduction
varied considerably with test allele used, in a manner analogous to the results
in these strains for base repair substitution test alleles. The general
features of UV-induced frameshift and substitution mutagenesis therefore appear
quite similar, indicating that they may depend on related processes. If this
conclusion is correct, greater attention must be given to integrating models
which account for the production of nucleotide additions and deletions into
those concerning misrepair mutagenesis.
MeSH Terms:
Base Composition/radiation effects
Base Sequence/radiation effects
Genes, Fungal/*radiation effects
*Mutation
Saccharomyces cerevisiae/*genetics/radiation effects
Support, U.S. Gov't, Non-P.H.S.
Support, U.S. Gov't, P.H.S.
*Ultraviolet Rays
Radiats Biol Radioecol 34: 336-341 (1994) [94348584]
[Fast repair in diploid yeast cells after combined exposure to ionizing
radiation with different LET]
N. M. Kabakova & V. G. Videnskii
Fast repair in diploid yeast cells Saccharomyces cerevisiae XS800 exposed to
the combined irradiation (alpha-particles + high-velocity electrons) was
studied. It has been shown that fast repair was significantly more effective
after combined irradiation with high doses than after exposure to high-velocity
electrons or alpha-particles alone. The regions of radioresistance in the cell
survival curves after combined irradiation can be explained by fast post-
irradiation repair.
MeSH Terms:
Alpha Particles
Cell Survival
Comparative Study
Diploidy
Electrons
Energy Transfer
English Abstract
Radiation Dosage
*Radiation, Ionizing
Saccharomyces cerevisiae/cytology/*radiation effects
Mutat Res 232: 327-36 (1990) [91015172]
Analysis of interactions between mutagens, II. Ethyl methanesulfonate and
ultraviolet light in Saccharomyces cerevisiae.
D. D. Ager & R. H. Haynes
Department of Biology, York University, Toronto, Ont., Canada.
The results of this study indicate the existence of a strong interaction
between ethyl methanesulfonate (EMS) and ultraviolet light (UV) for cell
killing in the yeast Saccharomyces cerevisiae. Conversely, mutation and gene
conversion frequencies observed for the combined treatment of EMS and UV do not
deviate significantly from that expected on the basis of simple additivity.
Studies involving repair-deficient mutants (rad mutants) reveal that the
synergistic interaction for cell killing depends on RAD52 function
(recombinational repair), but not on RAD3 function (excision repair). On the
basis of this analysis, the interaction between EMS and UV in S. cerevisiae
might arise from the inhibition of double-strand break repair by one, or both
agents.
MeSH Terms:
Cell Survival
Ethyl Methanesulfonate/*toxicity
Gene Conversion
Genes, Fungal/drug effects/radiation effects
Genes, Lethal/drug effects/radiation effects
Kinetics
Mutagens
Mutation/*drug effects/*radiation effects
Recombination, Genetic/drug effects/radiation effects
Saccharomyces cerevisiae/drug effects/*genetics/radiation effects
*Ultraviolet Rays
Gene Symbols:
ARG4-4
ARG4-17
HIS4-519
LEU2-3
LYS1-1
PET1
ADE2-18
URA3-52
ADE2-40
ILV1-92
TRP5-12
RAD52
TRR5-27
ADE2-119
Substances:
Ethyl Methanesulfonate (CAS 62-50-0)
Mutagens
Mutat Res 41: 241-8 (1976) [77100104]
The relation between repair of DNA and radiation and chemical mutagenesis in
Saccharomyces cerevisiae.
L. Prakash
The effect of various genes involved in DNA repair functions on radiation and
chemical mutagenesis in Escherichia coli is discussed and compared to similar
studies done in yeast. Results of the effect of various genes conferring
radiation-sensitivity on mutation induction in yeast are presented and related
to current ideas of mutagenesis.
MeSH Terms:
Comparative Study
*DNA Repair
Drug Resistance, Microbial
*Escherichia coli/drug effects/radiation effects
Genes
*Mutation
Radiation Tolerance
*Saccharomyces cerevisiae/radiation effects
Species Specificity
Support, U.S. Gov't, Non-P.H.S.
Support, U.S. Gov't, P.H.S.
Genetika 27: 1342-9 (1991) [92104477]
[Genetic instability of colonies' morphologic characteristics in the yeast
Saccharomyces cerevisiae. The influence of mutations of radiosensitivity]
V. M. Glazer, S. P. Soldatov, A. V. Glazunov, A. P. Morzunov & A. V. Boreiko
The exposure to ionizing radiation of radiosensitive mutants of diploid yeast
Saccharomyces cerevisiae deficient in double-strand break repair results in
formation of morphologically unstable colonies. Some characteristics of this
process were studied. The results obtained are consistent with the hypothesis
on relationship between DNA double-strand breaks or their repair with the
formation of unstable clones of diploid yeast cells.
MeSH Terms:
DNA Repair/genetics
Diploidy
English Abstract
Gene Rearrangement/genetics
Genes, Fungal/*radiation effects
Mutation
Radiation Tolerance/*genetics
Saccharomyces cerevisiae/*genetics
Radiobiologiia 30: 3-15 (1990) [90193082]
[The role of the repair of double-stranded DNA breaks in the radioresistance of
yeast cells]
A. V. Glazunov
The role of DNA double-strand break (DSB) repair in radioresistance of
Saccharomyces cerevisiae G1 cells is discussed. The contribution of rapid and
slow DNA DSB repair to radioresistance of diploid yeast has been estimated. The
contribution of the DNA DSB repair involving no homologous chromosome
interaction is shown to be insignificant in comparison with the recombinational
repair. The rapid DNA DSB repair efficiency calculation method based on the
proposed yeast radiation inactivation model is given. The calculations are in a
satisfactory agreement with the experimental data. Possible mechanisms of
radiation induction of lethal sectoring in yeast are discussed. This phenomenon
is supposed to be due to the DNA DSB processing during vegetative division of
irradiated cells. A general scheme of radiation inactivation of yeast cells is
proposed.
MeSH Terms:
DNA/*radiation effects
*DNA Damage
DNA Repair/*radiation effects
DNA, Fungal/*radiation effects
Dose-Response Relationship, Radiation
English Abstract
Interphase/radiation effects
Mutation
*Radiation Tolerance
Yeasts/*radiation effects
Substances:
DNA (CAS 9007-49-2)
DNA, Fungal
Mutat Res 160: 207-14 (1986) [86174826]
The rad2 mutation affects the molecular nature of UV and acridine-mustard-
induced mutations in the ADE2 gene of Saccharomyces cerevisiae.
E. L. Ivanov, S. V. Kovaltzova, G. V. Kassinova, L. M. Gracheva, V. G. Korolev
& I. A. Zakharov
We have studied the molecular nature of ade2 mutations induced by UV light and
bifunctional acridine-mustard (BAM) in wild-type (RAD) and in excision-
deficient (rad2) strains of the yeast, Saccharomyces cerevisiae. In the RAD
strain, UV causes 45% GC----AT transitions among all mutations; in the rad2
strain this value is 77%. BAM was shown to be highly specific for frameshift
mutagenesis: 60% frameshifts in the RAD strain, and as many as 84% frameshifts
in the rad2 strain were induced. Therefore, the rad2 mutation affects the
specificity of UV- and BAM-induced mutagenesis in yeast. Experimental data
agree with the view that the majority of mutations in the RAD strain are
induced by a prereplicative mechanism, whereas mutations in the RAD strain are
induced by a prereplicative mechanism, whereas mutations in the rad2 strain are
predominantly postreplicative events. Our results also suggest that: cytosine-
containing photoproducts are the substances responsible for major premutational
damage to cytosine-containing photoproducts are the substances responsible for
major premutational damage to DNA; a fraction of the mutations may arise in the
course of excision repair of UV photoproducts.
MeSH Terms:
DNA Repair
DNA Replication
Dose-Response Relationship, Radiation
*Genes, Fungal/drug effects/radiation effects
ICR 170/*pharmacology
Mutation
Nitrogen Mustard Compounds/*pharmacology
Radiation Tolerance
Saccharomyces cerevisiae/drug effects/*genetics/radiation effects
Suppression, Genetic
Ultraviolet Rays
Substances:
Nitrogen Mustard Compounds
ICR 170 (CAS 146-59-8)
Mutat Res 184: 197-207 (1987) [88038944]
Induction and repair of closely opposed pyrimidine dimers in Saccharomyces
cerevisiae.
R. J. Reynolds
Laboratory of Radiobiology, Harvard University School of Public Health, Boston,
MA 02115.
Pyrimidine dimer-DNA glycosylase activity prepared from Micrococcus luteus has
been used to develop an enzyme-sensitive site assay for the detection and
quantification of closely opposed pyrimidine dimers in the nuclear DNA of UV-
irradiated yeast. With this assay, closely opposed dimers were found to be
induced as a linear function of dose from 0 to 200 J/m2 (254 nm). Closely
opposed dimer frequencies decreased during the incubation of UV-irradiated,
excision repair-proficient cells under liquid-holding conditions in the dark
and during post-irradiation exposure of excision-deficient cells to
photoreactivating light. Incubation of excision-deficient cells in the dark had
no effect on the frequency of closely opposed dimers for up to 16 h. These
results indicate that closely opposed dimers in UV-irradiated yeast are subject
to repair by enzymatic photoreactivation and/or by dark-repair processes
dependent, at least in part, upon functions necessary for normal excision
repair. The genetic and biochemical implications of these results are discussed.
MeSH Terms:
*DNA Damage
*DNA Repair/radiation effects
DNA, Fungal/genetics/*radiation effects
Dose-Response Relationship, Radiation
Nucleosidases/metabolism
Pyrimidine Dimers/*metabolism
Saccharomyces cerevisiae/*genetics
Support, Non-U.S. Gov't
Support, U.S. Gov't, P.H.S.
Ultraviolet Rays
Substances:
Nucleosidases (EC 3.2.2.)
DNA, Fungal
Pyrimidine Dimers
DNA N-glycosidase (EC 3.2.2.-)
Mutat Res 129: 3-11 (1984) [85036439]
Inducibility of error-prone DNA repair in yeast?
W. Siede & F. Eckardt
Whereas some experimental evidence suggests that mutagenesis in yeast after
treatment with DNA-damaging agents involves inducible functions, a general-
acting error-prone repair activity analogous to the SOS system of Escherichia
coli has not yet been demonstrated. The current literature on the problem of
inducibility of mutagenic repair in yeast is reviewed with emphasis on the
differences in the experimental procedures applied.
MeSH Terms:
*DNA Repair
Dose-Response Relationship, Radiation
Enzyme Induction
Fungal Proteins/biosynthesis
Kinetics
*Mutation/radiation effects
Recombination, Genetic/radiation effects
Saccharomyces cerevisiae/*genetics
Ultraviolet Rays
Substances:
Fungal Proteins
Crit Rev Biotechnol 7: 281-337 (1988) [89119577]
Nonconventional yeasts: their genetics and biotechnological applications.
H. Weber & G. Barth
Central Institute of Microbiology and Experimental Therapy, Academy of Science
GDR, Jena.
To date, more than 500 species of yeasts have been described. Most of the
genetic and biochemical studies have, however, been carried out with
Saccharomyces cerevisiae. Although a considerable amount of knowledge has been
accumulated on fundamental processes and biotechnological applications of this
industrially important yeast, the large variety of other yeast genera and
species may offer various advantages for experimental study as well as for
product formation in biotechnology. The genetic investigation of these so-
called unconventional yeasts is poorly developed and information about
corresponding data is dispersed. It is the aim of this review to summarize and
discuss the main results of genetic studies and biotechnological applications
of unconventional yeasts and to serve as a guide for scientists who wish to
enter this field or are interested in only some aspects of these yeasts.
MeSH Terms:
*Biotechnology
Cloning, Molecular/methods
Crosses, Genetic
DNA, Fungal
Forecasting
Hybridization
Mutation
Nomenclature
Transformation, Genetic
Yeasts/*genetics/growth & development/physiology
Substances:
DNA, Fungal
Mutat Res 74: 439-58 (1980) [81122939]
Quantitative measures of mutagenicity and mutability based on mutant yield data.
F. Eckardt & R. H. Haynes
We described how mutant yield data (mutants per cell treated) can be used both
to compare the mutagenicity of different mutagens, and to characterize the
mutability of different cell types. Yield curves reveal the net effect of the
lethal and genetic actions of mutagens on cells. Normally, yields are the
quantities measured in assays for mutagenesis, and rectilinear plots of such
data baldly reveal the amount of experimental error and the extent of actual
mutant induction above the background level. Plots of yield versus lethal hits
can be used to quantify the relative mutagenic efficiency (RME) of agents whose
physical exposure doses otherwise would be incommensurable, as well as the
relative mutability (Rmt) of different strains to the same mutagen. Plots of
yield versus log dose provide an unambiguous way of assessing the relative
mutational sensitivities (Rms) and mutational resolutions (Rmr) of different
strains against a given mutagen. Such analysis is important for evaluation of
the relative merits of excision-proficient and excision-deficient strains of
the same organism as mutagen-testing systems. The mathematical approach
outlined here is applied, by way of example, to measurements of UV and 4-NQO
induced mutagenesis in both repair-deficient and repair-proficient haploid
strains of the yeast Saccharomyces cerevisiae.
MeSH Terms:
4-Nitroquinoline-1-oxide/pharmacology
Dose-Response Relationship, Drug
Dose-Response Relationship, Radiation
Mathematics
*Models, Genetic
*Mutagens
*Mutation
Saccharomyces cerevisiae/drug effects/genetics/radiation effects
Support, Non-U.S. Gov't
Ultraviolet Rays
Substances:
4-Nitroquinoline-1-oxide (CAS 56-57-5)
Mutagens
Curr Genet 18: 175-9 (1990) [91064750]
Role of the CDC8 gene in the repair of single strand breaks in DNA of the yeast
Saccharomyces cerevisiae.
H. Baranowska, D. Zaborowska, W. J. Jachymczyk & J. Zuk
Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Warsaw.
It has been found that the repair of single strand breaks is defective in the
DNA replication mutants cdc8-1 and cdc8-3 of Saccharomyces cerevisiae both in
permissive (23 degrees C) and restrictive conditions (36 degrees C). In
permissive conditions we observed a significant delay in single strand break
repair in a diploid strain HB7 (cdc8-1/cdc8-1), as compared with the wild-type
strain. Under restrictive conditions no repair was observed, but rather
degradation of MMS-damaged DNA occurred. It has been also found that the repair
of single strand breaks in yeast is inhibited by cycloheximide but not by
hydroxyurea.
MeSH Terms:
Centrifugation, Density Gradient
Cycloheximide/pharmacology
*DNA Repair/drug effects
DNA, Fungal/drug effects
Diploidy
Genes, Fungal
Hydroxyurea/pharmacology
Methyl Methanesulfonate/pharmacology
Saccharomyces cerevisiae/*genetics
Support, Non-U.S. Gov't
Temperature
Gene Symbols:
CDC8
Substances:
Cycloheximide (CAS 66-81-9)
Methyl Methanesulfonate (CAS 66-27-3)
Hydroxyurea (CAS 127-07-1)
DNA, Fungal
Genetics 95: 63-80 (1980) [81044897]
Heteroduplex repair as an intermediate step of UV mutagenesis in yeast.
F. Eckardt, S. J. Teh & R. H. Haynes
We have measured UV-induced mutation frequencies in yeast in a forward,
nonselective assay system by scoring white adex ade2 double auxotrophs among
parental red-pigmented ade2 clones. The frequencies of sectored and pure mutant
clones were determined separately. In excision-defective strains carrying the
genes rad1-1, rad3-2 and rad4-4, as well as in the double mutants, rad 1-1 rad
3-2 and rad 1-1 rad 4-4, considerably more sectored than pure clones are
induced in the low-dose range; in repair-competent strains, pure mutant clones
substantially outnumber the sectored clones. These results can be explained on
the basis of known differences in the timing of error-prone repair during the
cell division cycle; that is, we assume that error-prone repair occurs
primarily before replication in RAD wild-type strains but after replication in
excision-deficient mutants. It has been suggested that excision deficiency has
a pleiotropic effect on heteroduplex repair and nucleotide excision repair;
however, the high percentage (36.6%) of half-sectored clones found in the rad1-
1 strain is hard to reconcile with this hypothesis. We propose that
heteroduplex repair occurs subsequent to error-prone repair in both excision-
proficient and excision-deficient strains.
MeSH Terms:
Clone Cells/metabolism
*DNA Repair
DNA, Fungal/metabolism/*radiation effects
*Mutation
Pyrimidine Dimers/genetics
Saccharomyces cerevisiae/*genetics
Support, Non-U.S. Gov't
Ultraviolet Rays
Substances:
DNA, Fungal
Pyrimidine Dimers
Mol Cell Biol 6: 3555-8 (1986) [87089693]
Excision repair functions in Saccharomyces cerevisiae recognize and repair
methylation of adenine by the Escherichia coli dam gene.
M. F. Hoekstra & R. E. Malone
Unlike the DNA of higher eucaryotes, the DNA of Saccharomyces cerevisiae
(bakers' yeast) is not methylated. Introduction of the Escherichia coli dam
gene into yeast cells results in methylation of the N-6 position of adenine.
The UV excision repair system of yeast cells specifically responds to the
methylation, suggesting that it is capable of recognizing modifications which
do not lead to major helix distortion. The UV repair functions examined in this
report are involved in the incision step of pyrimidine dimer repair. These
observations may have relevance to the rearrangements and recombination events
observed when yeast or higher eucaryotic cells are transformed or transfected
with DNA grown in E. coli.
MeSH Terms:
Adenine
*DNA Repair
DNA Restriction Enzymes
Escherichia coli/*genetics
*Genes, Bacterial
Genotype
Methylation
Plasmids
Saccharomyces cerevisiae/*genetics
Support, Non-U.S. Gov't
Support, U.S. Gov't, Non-P.H.S.
Support, U.S. Gov't, P.H.S.
Substances:
DNA Restriction Enzymes (EC 3.1.21.)
Adenine (CAS 73-24-5)
Plasmids
Mutat Res 315: 281-293 (1994) [95059178]
Roles for the yeast RAD18 and RAD52 DNA repair genes in UV mutagenesis.
J. D. Armstrong, D. N. Chadee & B. A. Kunz
Microbiology Department, University of Manitoba, Winnipeg, Canada.
Experimental evidence indicates that although the Saccharomyces cerevisiae
RAD18 and RAD52 genes are not required for nucleotide excision repair, they
function in the processing of UV-induced DNA damage in yeast. Conflicting
statements regarding the UV mutability of strains deleted for RAD18 prompted us
to re-examine the influence of RAD18, and RAD52, on UV mutagenesis. To do so,
we characterized mutations induced by UV in SUP4-o, a yeast suppressor tRNA
gene. SUP4-o was maintained on a plasmid in isogenic strains that either
carried one of two different rad18 deletions (rad18 delta) or had RAD52
disrupted. Both rad18 deletions decreased the frequency of UV-induced SUP4-o
mutations to levels close to those for spontaneous mutagenesis in the rad18
delta backgrounds, and prevented a net increase in mutant yield. A detailed
analysis of mutations isolated after UV irradiation of one of the rad18 delta
strains uncovered little evidence of the specificity features typical for UV
mutagenesis in the isogenic repair-proficient (RAD) parent (e.g., predominance
of G.C-->A.T transitions). Evidently, UV induction of SUP4-o mutations is
highly dependent on the RAD18 gene. Compared to the RAD strain, disruption of
RAD52 reduced the frequency and yield of UV mutagenesis by about two-thirds.
Closer inspection revealed that 80% of this reduction was due to a decrease in
the frequency of G.C-->A.T transitions. In addition, there were differences in
the distributions and site specificities of single base-pair substitutions.
Thus, RAD52 also participates in UV mutagenesis of a plasmid-borne gene in
yeast, but to a lesser extent than RAD18.
MeSH Terms:
Base Sequence
DNA Mutational Analysis
DNA Repair/*genetics
DNA, Fungal/radiation effects
DNA-Binding Proteins/*genetics
Fungal Proteins/*genetics
Genes, Fungal/radiation effects
Genes, Suppressor/genetics
Molecular Sequence Data
*Mutagenesis
Point Mutation/genetics
RNA, Transfer/genetics
Saccharomyces cerevisiae/*genetics
Sequence Deletion/physiology
Support, Non-U.S. Gov't
*Ultraviolet Rays
Gene Symbols:
RAD52
RAD18
Substances:
RNA, Transfer (CAS 9014-25-9)
DNA-Binding Proteins
DNA, Fungal
Fungal Proteins
RAD18 protein
Rad52 protein
Mutat Res 191: 9-12 (1987) [87201647]
UV response of the temperature-conditional rad 54 mutant of the yeast
Saccharomyces cerevisiae.
J. Kiefer
The survival of the yeast mutant rad 54-3, which is temperature-conditional for
the repair of double-strand breaks, was measured after exposure to UV-light
(254 nm) and incubation at 23 degrees C and 36 degrees C. It was found that
survival was drastically reduced with incubation at the restrictive
temperature. Temperature-shift experiments indicated that repair of UV-induced
damage which is controlled by the rad 54 gene proceeds with a half-value-time
of about 7 h.
MeSH Terms:
*DNA Damage
*DNA Repair
Dose-Response Relationship, Radiation
Genes, Fungal
Mutation
Saccharomyces cerevisiae/genetics/*radiation effects
Temperature
Ultraviolet Rays
Genetics 92: 83-97 (1979) [80047781]
Mutagenesis by cytostatic alkylating agents in yeast strains of differing
repair capacities.
A. Ruhland & M. Brendel
Reversion of two nulcear ochre nonsense alleles and cell inactivation induced
by mono-, bi-, and tri-functional alkylating agents and by UV has been
investigated in stationary-phase haploid cells of yeast strains with differing
capacities for DNA repair. The ability to survive alkylation damage is
correlated with UV repair capacity, a UV-resistant and UV-mutable strain (RAD
REV) being least and a UV-sensitive and UV-nonmutable strain (radi rev3) most
sensitive. Mutagenicity of alkylating agents is highest in the former and is
abolished in the latter strain. Deficiency in excision repair (rad1 rad2) or in
the RAD18 function does not lead to enhanced mutability. Mutagenesis by the
various agents is characterized by a common pattern of induction of locus-
specific revertants and suppressor mutants. Induction kinetics are mostly
linear, but UV-induced reversion in the RAD REV strain follows higher-than-
linear (probably "quadratic") kinetics. The alkylating agent cyclophosphamide,
usually considered inactive without metabolic conversion, reduces colony-
forming ability and induces revertants in a manner similar but not identical to
the other chemicals tested. These findings are taken to support the concept of
mutagenesis by misrepair after alkylation, which albeit sharing common features
with the mechanism of UV-induced reversion, can be distinguished therefrom.
MeSH Terms:
Alkylating Agents/*pharmacology
*DNA Repair
DNA Replication
DNA, Fungal/*genetics/radiation effects
Genotype
Phenotype
Saccharomyces cerevisiae/*genetics/radiation effects
Ultraviolet Rays
Mol Gen Genet 186: 1-9 (1982) [82271431]
The mechanism of untargeted mutagenesis in UV-irradiated yeast.
C. W. Lawrence & R. B. Christensen
The SOS error-prone repair hypothesis proposes that untargeted and targeted
mutations in E. coli both result from the inhibition of polymerase functions
that normally maintain fidelity, and that this is a necessary precondition for
translesion synthesis. Using mating experiments with excision deficient strains
of Bakers' yeast, Saccharomyces cerevisiae, we find that up to 40% of cycl-91
revertants induced by UV are untargeted, showing that a reduction in fidelity
is also found in irradiated cells of this organism. We are, however, unable to
detect the induction or activation of any diffusible factor capable of
inhibiting fidelity, and therefore suggest that untargeted and targeted
mutations are the consequence of largely different processes. We propose that
these observations are best explained in terms of a limited fidelity model.
Untargeted mutations are thought to result from the limited capacity of
processes which normally maintain fidelity, which are active during replication
on both irradiated and unirradiated templates. Even moderate UV fluences
saturate this capacity, leading to competition for the limited resource.
Targeted mutations are believed to result from the limited, though far from
negligible, capacity of lesions like pyrimidine dimers to form Watson-Crick
base pairs.
MeSH Terms:
Crosses, Genetic
Genotype
*Mutation
Saccharomyces cerevisiae/genetics/growth & development/*radiation effects
Support, U.S. Gov't, P.H.S.
*Ultraviolet Rays
Biochemistry 31: 3694-702 (1992) [92232657]
Excision repair of DNA in nuclear extracts from the yeast Saccharomyces
cerevisiae.
Z. Wang, X. Wu & E. C. Friedberg
Department of Pathology, University of Texas Southwestern Medical Center,
Dallas 75235.
Excision repair of DNA is an important cellular response to DNA damage caused
by a broad spectrum of physical and chemical agents. We have established a cell-
free system in which damage-specific DNA repair synthesis can be demonstrated
in vitro with nuclear extracts from the yeast Saccharomyces cerevisiae. Repair
synthesis of UV-irradiated plasmid DNA was observed in a radiation dose-
dependent manner and was unaffected by mutations in the RAD1, RAD2, RAD3, RAD4,
RAD10, or APN1 genes. DNA damaged with cis-platin was not recognized as a
substrate for repair synthesis. Further examination of the repair synthesis
observed with UV-irradiated DNA revealed that it is dependent on the presence
of endonuclease III-sensitive lesions in DNA, but not pyrimidine dimers. These
observations suggest that the repair synthesis observed in yeast nuclear
extracts reflects base excision repair of DNA. Our data indicate that the patch
size of this repair synthesis is at least seven nucleotides. This system is
expected to facilitate the identification of specific gene products which
participate in base excision repair in yeast.
MeSH Terms:
Cell Nucleus/metabolism/radiation effects
Cell-Free System
Cisplatin/toxicity
DNA
DNA Damage
*DNA Repair
Genes, Fungal
Human
Mutation
Plasmids
Pyrimidine Dimers/genetics
Saccharomyces cerevisiae/*genetics/radiation effects
Support, U.S. Gov't, P.H.S.
Gene Symbols:
RAD
Substances:
DNA (CAS 9007-49-2)
Cisplatin (CAS 15663-27-1)
Plasmids
Pyrimidine Dimers
Mol Gen Genet 177: 541-4 (1980) [80187587]
A new mutant of the yeast Saccharomyces cerevisiae defective in excision of UV-
damaged sites in DNA.
M. L. Bekker, O. K. Kaboev & S. V. Koval'tsova
An UV-sensitive yeast mutant, uvs12, with almost unchanged sensitivity to gamma-
irradiation and methylmethane sulphonate was obtained. uvs12, non allelic to
any of the known UV-sensitive mutants from radI to rad21 is defective in early
steps of excision repair. This inference is based on the fact that after 4-5 h
post-irradiation incubation unexcised pyrimidine dimers are retained in nuclear
DNA, which follows from two independent tests: the retention of UV-
endonuclease-sensitive sites and enhanced survival after photoreactivation.
MeSH Terms:
*DNA Repair/radiation effects
DNA, Fungal/genetics/radiation effects
Gamma Rays
Light
*Mutation
Phenotype
Pyrimidine Dimers/radiation effects
Saccharomyces cerevisiae/*genetics
Ultraviolet Rays
Substances:
DNA, Fungal
Pyrimidine Dimers
Mutat Res 30: 209-18 (1975) [76100545]
Repair of UV-induced DNA damage and survival in yeast. I. Dimer excision.
R. Wheatcroft, B. S. Cox & R. H. Haynes
The amount of pyrimidine dimer UV photoproduct lost from the DNA of irradiated
yeast cells during dark incubation has been measured in various conditions. It
was found that no dimers were lost when cells were incubated in saline. When
the cells were incubated, with aeration, in a full growth medium, dimers were
lost, most excision being complete within 4 h. Not all dimers were lost and the
number lost was a function of UV dose. Maximum loss, amounting to 50 000 dimers
per genome was observed after 4000 or 6000 erg/mm2 of UV. At higher doses, the
number excised declined. Making the assumptions that dimers are the principal
lethal product of UV, that a single dimer remaining in its genome is enough to
prevent a cell from multiplying and that excision is the principal dark-repair
process in yeast, these data were incorporated into the repair term of an
expression relating survival to repair8 and it was found that the survival of
yeast at doses up to 2000 erg/mm2 of UV could be quite accurately predicted.
This is the first time it has been possible to account for survival in terms of
measured repair. It is suggested that the divergence of the predicted and
observed curves at higher doses is due to other processes known to exist in
yeast.
MeSH Terms:
*DNA Repair
Dose-Response Relationship, Radiation
Haploidy
*Polymers
*Pyrimidines
Radiation Genetics
Saccharomyces cerevisiae/*physiology/radiation effects
Ultraviolet Rays
