UBC13 , a DNA-damage-inducible gene, is a member of the error-free postreplication repair pathway in Saccharomyces cerevisiae

2000 ◽  
Vol 37 (3) ◽  
pp. 168-174 ◽  
Author(s):  
Janna Brusky ◽  
Yu Zhu ◽  
Wei Xiao
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Damage ◽  
Repair Pathway ◽  
Postreplication Repair ◽  
Inducible Gene

scholarly journals The Product of the DNA Damage-Inducible Gene of Saccharomyces cerevisiae, DIN7, Specifically Functions in Mitochondria

Genetics ◽  
2000 ◽  
Vol 154 (1) ◽  
pp. 73-81 ◽  
Author(s):  
Marta U Fikus ◽  
Piotr A Mieczkowski ◽  
Piotr Koprowski ◽  
Joanna Rytka ◽  
Ewa Śledziewska-Gójska ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Damage ◽  
Transcriptional Activation ◽  
Fluorescent Protein ◽  
Cell Fractionation ◽  
Gal1 Promoter ◽  
Green Fluorescent ◽  
Inducible Genes ◽  
Chromosomal Mutations ◽  
Inducible Gene

Abstract We reported previously that the product of the DNA damage-inducible gene of Saccharomyces cerevisiae, DIN7, belongs to a family of proteins that are involved in DNA repair and replication. The family includes S. cerevisiae proteins Rad2p and its human homolog XPGC, Rad27p and its mammalian homolog FEN-1, and Exonuclease I (Exo I). Here, we report that Din7p specifically affects metabolism of mitochondrial DNA (mtDNA). We have found that dun1 strains, defective in the transcriptional activation of the DNA damage-inducible genes RNR1, RNR2, and RNR3, exhibit an increased frequency in the formation of the mitochondrial petite (ρ−) mutants. This high frequency of petites arising in the dun1 strains is significantly reduced by the din7::URA3 allele. On the other hand, overproduction of Din7p from the DIN7 gene placed under control of the GAL1 promoter dramatically increases the frequency of petite formation and the frequency of mitochondrial mutations conferring resistance to erythromycin (Er). The frequencies of chromosomal mutations conferring resistance to canavanine (Canr) or adenine prototrophy (Ade+) are not affected by enhanced synthesis of Din7p. Experiments using Din7p fused to the green fluorescent protein (GFP) and cell fractionation experiments indicate that the protein is located in mitochondria. A possible mechanism that may be responsible for the decreased stability of the mitochondrial genome in S. cerevisiae cells with elevated levels of Din7p is discussed.

Enhanced expression of the DNA damage-inducible gene DIN7 results in increased mutagenesis of mitochondrial DNA in Saccharomyces cerevisiae

2003 ◽  
Vol 269 (5) ◽  
pp. 632-639 ◽  
Author(s):  
P. Koprowski ◽  
M. U. Fikus ◽  
P. Dzierzbicki ◽  
P. Mieczkowski ◽  
J. Lazowska ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Damage ◽  
Mitochondrial Dna ◽  
Enhanced Expression ◽  
Inducible Gene

scholarly journals The Human F-Box DNA Helicase FBH1 Faces Saccharomyces cerevisiae Srs2 and Postreplication Repair Pathway Roles

2007 ◽  
Vol 27 (21) ◽  
pp. 7439-7450 ◽  
Author(s):  
Irene Chiolo ◽  
Marco Saponaro ◽  
Anastasia Baryshnikova ◽  
Jeong-Hoon Kim ◽  
Yeon-Soo Seo ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Damage ◽  
Self Regulation ◽  
Dna Helicase ◽  
Genome Integrity ◽  
Helicase Domain ◽  
Postreplication Repair ◽  
Scf Ubiquitin Ligase ◽  
Human Orthologue ◽  
Eukaryotic Organisms

ABSTRACTTheSaccharomyces cerevisiaeSrs2 UvrD DNA helicase controls genome integrity by preventing unscheduled recombination events. While Srs2 orthologues have been identified in prokaryotic and lower eukaryotic organisms, human orthologues of Srs2 have not been described so far. We found that the human F-box DNA helicase hFBH1 suppresses specific recombination defects ofS. cerevisiae srs2mutants, consistent with the finding that the helicase domain of hFBH1 is highly conserved with that of Srs2. Surprisingly, hFBH1 in the absence ofSRS2also suppresses the DNA damage sensitivity caused by inactivation of postreplication repair-dependent functions leading to PCNA ubiquitylation. The F-box domain of hFBH1, which is not present in Srs2, is crucial for hFBH1 functions in substituting for Srs2 and postreplication repair factors. Furthermore, our findings indicate that an intact F-box domain, acting as an SCF ubiquitin ligase, is required for the DNA damage-induced degradation of hFBH1 itself. Overall, our findings suggest that the hFBH1 helicase is a functional human orthologue of budding yeast Srs2 that also possesses self-regulation properties necessary to execute its recombination functions.

The DNA damage-inducible gene DIN1 of Saccharomyces cerevisiae encodes a regulatory subunit of ribonucleotide reductase and is identical to RNR3

1990 ◽  
Vol 10 (10) ◽  
pp. 5553-5557
Author(s):  
K Yagle ◽  
K McEntee
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Damage ◽  
Ribonucleotide Reductase ◽  
Regulatory Elements ◽  
Catalytic Subunit ◽  
Regulatory Subunit ◽  
Subunit Gene ◽  
Gene Encoding ◽  
Sequence Elements ◽  
Inducible Gene

The sequence of the DIN1 gene of Saccharomyces cerevisiae is identical to RNR3, a gene encoding a DNA damage-inducible regulatory subunit of ribonucleotide reductase. Two sequence elements located upstream of DIN1 (RNR3) are homologous to putative DNA damage regulatory elements in the promoter of the reductase catalytic subunit gene, RNR2. The transcript start sites for DIN1(RNR3) have been localized, and induction by different agents has been compared with other DNA damage-regulated genes.

scholarly journals The DNA damage-inducible gene DIN1 of Saccharomyces cerevisiae encodes a regulatory subunit of ribonucleotide reductase and is identical to RNR3.

1990 ◽  
Vol 10 (10) ◽  
pp. 5553-5557 ◽  
Author(s):  
K Yagle ◽  
K McEntee
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Damage ◽  
Ribonucleotide Reductase ◽  
Regulatory Elements ◽  
Catalytic Subunit ◽  
Regulatory Subunit ◽  
Subunit Gene ◽  
Gene Encoding ◽  
Sequence Elements ◽  
Inducible Gene

The sequence of the DIN1 gene of Saccharomyces cerevisiae is identical to RNR3, a gene encoding a DNA damage-inducible regulatory subunit of ribonucleotide reductase. Two sequence elements located upstream of DIN1 (RNR3) are homologous to putative DNA damage regulatory elements in the promoter of the reductase catalytic subunit gene, RNR2. The transcript start sites for DIN1(RNR3) have been localized, and induction by different agents has been compared with other DNA damage-regulated genes.

scholarly journals Radiosensitive and Mitotic Recombination Phenotypes of the Saccharomyces cerevisiae dun1 Mutant Defective in DNA Damage-Inducible Gene Expression

Genetics ◽  
1999 ◽  
Vol 152 (3) ◽  
pp. 909-919 ◽  
Author(s):  
Michael Fasullo ◽  
Joseph Koudelik ◽  
Peter AhChing ◽  
Peter Giallanza ◽  
Cinzia Cera
Keyword(s):  
Gene Expression ◽  
Saccharomyces Cerevisiae ◽  
Dna Damage ◽  
Biological Significance ◽  
Uv Damage ◽  
Triple Mutant ◽  
Inducible Gene Expression ◽  
Dna Damaging Agents ◽  
Inducible Gene

Abstract The biological significance of DNA damage-induced gene expression in conferring resistance to DNA-damaging agents is unclear. We investigated the role of DUN1-mediated, DNA damage-inducible gene expression in conferring radiation resistance in Saccharomyces cerevisiae. The DUN1 gene was assigned to the RAD3 epistasis group by quantitating the radiation sensitivities of dun1, rad52, rad1, rad9, rad18 single and double mutants, and of the dun1 rad9 rad52 triple mutant. The dun1 and rad52 single mutants were similar in terms of UV sensitivities; however, the dun1 rad52 double mutant exhibited a synergistic decrease in UV resistance. Both spontaneous intrachromosomal and heteroallelic gene conversion events between two ade2 alleles were enhanced in dun1 mutants, compared to DUN1 strains, and elevated recombination was dependent on RAD52 but not RAD1 gene function. Spontaneous sister chromatid exchange (SCE), as monitored between truncated his3 fragments, was not enhanced in dun1 mutants, but UV-induced SCE and heteroallelic recombination were enhanced. Ionizing radiation and methyl methanesulfonate (MMS)-induced DNA damage did not exhibit greater recombinogenicity in the dun1 mutant compared to the DUN1 strain. We suggest that one function of DUN1-mediated DNA damage-induced gene expression is to channel the repair of UV damage into a nonrecombinogenic repair pathway.

scholarly journals Withanolide D Enhances Radiosensitivity of Human Cancer Cells by Inhibiting DNA Damage Non-homologous End Joining Repair Pathway

2020 ◽  
Vol 9 ◽  
Author(s):  
Jerome Lacombe ◽  
Titouan Cretignier ◽  
Laetitia Meli ◽  
E. M. Kithsiri Wijeratne ◽  
Jean-Luc Veuthey ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cancer Cells ◽  
Human Cancer ◽  
Repair Pathway ◽  
End Joining ◽  
Human Cancer Cells ◽  
Non Homologous End Joining
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