The DNA repair gene PSO3 of Saccharomyces cerevisiae belongs to the RAD3 epistasis group

1992 ◽  
Vol 21 (1) ◽  
pp. 85-90 ◽  
Author(s):  
Mara S. Benfato ◽  
Martin Brendel ◽  
Jo�o A. P. Henriques
1989 ◽  
Vol 9 (8) ◽  
pp. 3314-3322
Author(s):  
G M Cole ◽  
R K Mortimer

The Saccharomyces cerevisiae RAD54 gene is transcriptionally regulated by a broad spectrum of DNA-damaging agents. Induction of RAD54 by DNA-damaging agents is under positive control. Sequences responsible for DNA damage induction (the DRS element) lie within a 29-base-pair region from -99 to -70 from the most proximal transcription start site. This inducible promoter element is functionally separable from a poly(dA-dT) region immediately downstream which is required for constitutive expression. Deletions which eliminate induction of RAD54 transcription by DNA damage but do not affect constitutive expression have no effect on growth or survival of noninducible strains relative to wild-type strains in the presence of DNA-damaging agents. The DRS element is also not required for homothallic mating type switching, transcriptional induction of RAD54 during meiosis, meiotic recombination, or spontaneous or X-ray-induced mitotic recombination. We find no phenotype for a lack of induction of RAD54 message via the damage-inducible DRS, which raises significant questions about the physiology of DNA damage induction in S. cerevisiae.


1995 ◽  
Vol 23 (10) ◽  
pp. 1679-1685 ◽  
Author(s):  
D. d. Bang ◽  
V. Timmermans ◽  
R. Verhage ◽  
A. M. Zeeman ◽  
P. van de Putte ◽  
...  

2000 ◽  
Vol 21 (6) ◽  
pp. 519-528 ◽  
Author(s):  
Zongrang Liu ◽  
Gazi Showkat Hossain ◽  
Maria A. Islas-Osuna ◽  
David L. Mitchell ◽  
David W. Mount

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Pengyao Jiang ◽  
Anja R Ollodart ◽  
Vidha Sudhesh ◽  
Alan J Herr ◽  
Maitreya J Dunham ◽  
...  

Although studies of Saccharomyces cerevisiae have provided many insights into mutagenesis and DNA repair, most of this work has focused on a few laboratory strains. Much less is known about the phenotypic effects of natural variation within S. cerevisiae's DNA repair pathways. Here, we use natural polymorphisms to detect historical mutation spectrum differences among several wild and domesticated S. cerevisiae strains. To determine whether these differences are likely caused by genetic mutation rate modifiers, we use a modified fluctuation assay with a CAN1 reporter to measure de novo mutation rates and spectra in 16 of the analyzed strains. We measure a 10-fold range of mutation rates and identify two strains with distinctive mutation spectra. These strains, known as AEQ and AAR, come from the panel's 'Mosaic beer' clade and share an enrichment for C>A mutations that is also observed in rare variation segregating throughout the genomes of several Mosaic beer and Mixed origin strains. Both AEQ and AAR are haploid derivatives of the diploid natural isolate CBS 1782, whose rare polymorphisms are enriched for C>A as well, suggesting that the underlying mutator allele is likely active in nature. We use a plasmid complementation test to show that AAR and AEQ share a mutator allele in the DNA repair gene OGG1, which excises 8-oxoguanine lesions that can cause C>A mutations if left unrepaired.


1989 ◽  
Vol 9 (4) ◽  
pp. 1794-1798 ◽  
Author(s):  
M van Duin ◽  
J van Den Tol ◽  
J H Hoeijmakers ◽  
D Bootsma ◽  
I P Rupp ◽  
...  

We report that the genes for the homologous Saccharomyces cerevisiae RAD10 and human ERCC-1 DNA excision repair proteins harbor overlapping antisense transcription units in their 3' regions. Since naturally occurring antisense transcription is rare in S. cerevisiae and humans (this is the first example in human cells), our findings indicate that antisense transcription in the ERCC-1-RAD10 gene regions represents an evolutionarily conserved feature.


1993 ◽  
Vol 13 (12) ◽  
pp. 7757-7765
Author(s):  
J F Watkins ◽  
P Sung ◽  
L Prakash ◽  
S Prakash

In eukaryotes, the posttranslational conjugation of ubiquitin to various cellular proteins marks them for degradation. Interestingly, several proteins have been reported to contain ubiquitin-like (ub-like) domains that are in fact specified by the DNA coding sequences of the proteins. The biological role of the ub-like domain in these proteins is not known; however, it has been proposed that this domain functions as a degradation signal rendering the proteins unstable. Here, we report that the product of the Saccharomyces cerevisiae RAD23 gene, which is involved in excision repair of UV-damaged DNA, bears a ub-like domain at its amino terminus. This finding has presented an opportunity to define the functional significance of this domain. We show that deletion of the ub-like domain impairs the DNA repair function of RAD23 and that this domain can be functionally substituted by the authentic ubiquitin sequence. Surprisingly, RAD23 is highly stable, and the studies reported herein indicate that its ub-like domain does not mediate protein degradation. Thus, in RAD23 at least, the ub-like domain affects protein function in a nonproteolytic manner.


1995 ◽  
Vol 15 (12) ◽  
pp. 7067-7080 ◽  
Author(s):  
A R Lehmann ◽  
M Walicka ◽  
D J Griffiths ◽  
J M Murray ◽  
F Z Watts ◽  
...  

The rad18 mutant of Schizosaccharomyces pombe is very sensitive to killing by both UV and gamma radiation. We have cloned and sequenced the rad18 gene and isolated and sequenced its homolog from Saccharomyces cerevisiae, designated RHC18. The predicted Rad18 protein has all the structural properties characteristic of the SMC family of proteins, suggesting a motor function--the first implicated in DNA repair. Gene deletion shows that both rad18 and RHC18 are essential for proliferation. Genetic and biochemical analyses suggest that the product of the rad18 gene acts in a DNA repair pathway for removal of UV-induced DNA damage that is distinct from classical nucleotide excision repair. This second repair pathway involves the products of the rhp51 gene (the homolog of the RAD51 gene of S. cerevisiae) and the rad2 gene.


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