Ultraviolet light induced mutagenesis of mitochondrial genes in the rad6, rev3 and cdc8 mutants of Saccharomyces cerevisiae

1983 ◽  
Vol 189 (3) ◽  
pp. 513-515 ◽  
Author(s):  
Renata Polakowska ◽  
Louise Prakash ◽  
Satva Prakash
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Ultraviolet Light ◽  
Mitochondrial Genes ◽  
Induced Mutagenesis

RAD6+ gene of Saccharomyces cerevisiae codes for two mutationally separable deoxyribonucleic acid repair functions

1981 ◽  
Vol 1 (2) ◽  
pp. 153-157
Author(s):  
M F Tuite ◽  
B S Cox
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Ultraviolet Light ◽  
Deoxyribonucleic Acid ◽  
Lethal Effects ◽  
Rad6 Gene ◽  
Ultraviolet Sensitivity ◽  
Induced Mutagenesis ◽  
Error Prone Repair

The response of two mutant alleles of the RAD6+ gene of Saccharomyces cerevisiae to the ochre translational suppressor SUQ5 was determined. Both the ultraviolet sensitivity phenotype and the deficiency in ultraviolet-induced mutagenesis phenotype of the rad6-1 allele were suppressed in a [psi+] background. For the rad6-3 allele, only the ultraviolet-sensitivity phenotype was suppressible in a [psi+] background. An SUQ5 rad6-3 [psi+] strain that was examined showed the normal rad6-3 deficiency in ultraviolet-induced mutagenesis. We propose that the RAD6+ gene is divided into two cistrons, RAD6A and RAD6B. RAD6A codes for an activity responsible for the error-prone repair of ultraviolet-induced lesions in deoxyribonucleic acid but is not involved in a cell's resistance to the lethal effects of ultraviolet light. RAD6B codes for an activity essential for error-free repair of potentially lethal mutagenic damage.

scholarly journals RAD6+ gene of Saccharomyces cerevisiae codes for two mutationally separable deoxyribonucleic acid repair functions.

1981 ◽  
Vol 1 (2) ◽  
pp. 153-157 ◽  
Author(s):  
M F Tuite ◽  
B S Cox
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Ultraviolet Light ◽  
Deoxyribonucleic Acid ◽  
Lethal Effects ◽  
Rad6 Gene ◽  
Ultraviolet Sensitivity ◽  
Induced Mutagenesis ◽  
Error Prone Repair

The response of two mutant alleles of the RAD6+ gene of Saccharomyces cerevisiae to the ochre translational suppressor SUQ5 was determined. Both the ultraviolet sensitivity phenotype and the deficiency in ultraviolet-induced mutagenesis phenotype of the rad6-1 allele were suppressed in a [psi+] background. For the rad6-3 allele, only the ultraviolet-sensitivity phenotype was suppressible in a [psi+] background. An SUQ5 rad6-3 [psi+] strain that was examined showed the normal rad6-3 deficiency in ultraviolet-induced mutagenesis. We propose that the RAD6+ gene is divided into two cistrons, RAD6A and RAD6B. RAD6A codes for an activity responsible for the error-prone repair of ultraviolet-induced lesions in deoxyribonucleic acid but is not involved in a cell's resistance to the lethal effects of ultraviolet light. RAD6B codes for an activity essential for error-free repair of potentially lethal mutagenic damage.

scholarly journals The SRS2 suppressor of rad6 mutations of Saccharomyces cerevisiae acts by channeling DNA lesions into the RAD52 DNA repair pathway.

Genetics ◽  
1990 ◽  
Vol 124 (4) ◽  
pp. 817-831 ◽  
Author(s):  
R H Schiestl ◽  
S Prakash ◽  
L Prakash
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Repair ◽  
Gamma Ray ◽  
Dna Lesions ◽  
Recombinational Repair ◽  
Repair Pathway ◽  
Uv Mutagenesis ◽  
Uv Sensitivity ◽  
Suppressor Mutations ◽  
Induced Mutagenesis

Abstract rad6 mutants of Saccharomyces cerevisiae are defective in the repair of damaged DNA, DNA damage induced mutagenesis, and sporulation. In order to identify genes that can substitute for RAD6 function, we have isolated genomic suppressors of the UV sensitivity of rad6 deletion (rad6 delta) mutations and show that they also suppress the gamma-ray sensitivity but not the UV mutagenesis or sporulation defects of rad6. The suppressors show semidominance for suppression of UV sensitivity and dominance for suppression of gamma-ray sensitivity. The six suppressor mutations we isolated are all alleles of the same locus and are also allelic to a previously described suppressor of the rad6-1 nonsense mutation, SRS2. We show that suppression of rad6 delta is dependent on the RAD52 recombinational repair pathway since suppression is not observed in the rad6 delta SRS2 strain containing an additional mutation in either the RAD51, RAD52, RAD54, RAD55 or RAD57 genes. Possible mechanisms by which SRS2 may channel unrepaired DNA lesions into the RAD52 DNA repair pathway are discussed.

Transcriptional analysis of the Saccharomyces cerevisiae mitochondrial var1 gene: anomalous hybridization of RNA from AT-rich regions

1983 ◽  
Vol 3 (9) ◽  
pp. 1615-1624
Author(s):  
H P Zassenhaus ◽  
F Farrelly ◽  
M E Hudspeth ◽  
L I Grossman ◽  
R A Butow
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mitochondrial Genes ◽  
Transcriptional Analysis ◽  
Asymmetric Distribution ◽  
Direct Function ◽  
Important Conclusion ◽  
The Family ◽  
Var1 Gene ◽  
Flanking Sequences ◽  
Transcription Map

A family of mitochondrial RNAs hybridizes specifically to the var1 region on Saccharomyces cerevisiae mitochondrial DNA (Farrelly et al., J. Biol. Chem. 257:6581-6587, 1982). We constructed a fine-structure transcription map of this region by hybridizing DNA probes containing different portions of the var1 region and some flanking sequences to mitochondrial RNAs isolated from var1-containing petites. We also report the nucleotide sequence of more than 1.2 kilobases of DNA flanking the var1 gene. Our primary findings are: (i) The family of RNAs we detect with homology to var1 DNA is colinear with the var1 gene. Their direction of transcription is olil to cap, as it is for most other mitochondrial genes. (ii) Extensive hybridization anomalies are present, most likely due to the high A-T (A-U) content of the hybridizing species and to the asymmetric distribution of their G-C residues. An important conclusion is that failure to detect transcripts from A-T-rich regions of the yeast mitochondrial genome by standard blot transfer hybridizations cannot be interpreted to mean that such sequences, which are commonly supposed to be spacer DNA, are noncoding or lack direct function in the expression of mitochondrial genes.

scholarly journals Structure-function relationships of the yeast cyclin-dependent kinase Pho85.

1995 ◽  
Vol 15 (10) ◽  
pp. 5482-5491 ◽  
Author(s):  
R C Santos ◽  
N C Waters ◽  
C L Creasy ◽  
L W Bergman
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Structure Function ◽  
Cell Cycle Progression ◽  
Substrate Recognition ◽  
The Other ◽  
Cyclin Dependent Kinase ◽  
Cycle Progression ◽  
Cyclin Dependent Kinases ◽  
Induced Mutagenesis

The PHO85 gene of Saccharomyces cerevisiae encodes a cyclin-dependent kinase involved in both transcriptional regulation and cell cycle progression. Although a great deal is known concerning the structure, function, and regulation of the highly homologous Cdc28 protein kinase, little is known concerning these relationships in regard to Pho85. In this study, we constructed a series of Pho85-Cdc28 chimeras to map the region(s) of the Pho85 molecule that is critical for function of Pho85 in repression of acid phosphatase (PHO5) expression. Using a combination of site-directed and ethyl methanesulfonate-induced mutagenesis, we have identified numerous residues critical for either activation of the Pho85 kinase, interaction of Pho85 with the cyclin-like molecule Pho80, or substrate recognition. Finally, analysis of mutations analogous to those previously identified in either Cdc28 or cdc2 of Schizosaccharomyces pombe suggested that the inhibition of Pho85-Pho80 activity in mechanistically different from that seen in the other cyclin-dependent kinases.

PURE AND MOSAIC CLONES — A REFLECTION OF DIFFERENCES IN MECHANISMS OF MUTAGENESIS BY DIFFERENT AGENTS IN SACCHAROMYCES CEREVISIAE

1981 ◽  
Vol 23 (1) ◽  
pp. 73-79 ◽  
Author(s):  
A. Nasim ◽  
M. A. Hannan ◽  
Earle R. Nestmann
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Ultraviolet Light ◽  
Nitrous Acid ◽  
Repair Process ◽  
Dna Lesions ◽  
Ethyl Methanesulfonate ◽  
Methyl Methanesulfonate ◽  
Mechanisms Of Mutagenesis ◽  
G1 Cells

The induction of pure and mosaic clones has been studied in haploid G1 cells of Saccharomyces cerevisiae. Following treatments with ultraviolet light, methyl methanesulfonate, ethyl methanesulfonate, nitrous acid, and N-methyl-N′-nitro-N-nitrosoguanidine, the relative proportions of pure mutant clones varied from 25 to 100% at comparable survival levels. Ultraviolet light and methyl methanesulfonate produced mainly pure mutant clones, whereas ethyl methanesulfonate and nitrous acid produced mainly mosaics at 59 to 100% survival levels. The ratio of pure to mosaic clones induced by nitrosoguanidine fell between these two classes. These results are consistent with a classification of mutagens on the basis of repair and replication-dependent mechanisms of mutagenesis in other organisms. Agents having actions similar to ultraviolet light may produce mainly pure clones through a pre-replicative process involving an error-prone DNA repair process. Others may produce mainly mosaic mutants due to the different nature of DNA lesions which may require a replication-dependent process for fixation of mutations. Preliminary data from combined treatments of mutagens belonging to two different classes (i.e. ultraviolet light and nitrous acid) suggest the possibility of an interaction between these agents, resulting in a higher proportion of pure clones, possibly due to an inducible process. Studies of induced frequencies of pure and mosaic clones may be useful in the characterization of mutagens with functional differences.

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