scholarly journals Regulatory and DNA Repair Genes Contribute to the Desiccation Resistance of Sinorhizobium meliloti Rm1021

2008 ◽  
Vol 75 (2) ◽  
pp. 446-453 ◽  
Author(s):  
Jodi L. Humann ◽  
Hope T. Ziemkiewicz ◽  
Svetlana N. Yurgel ◽  
Michael L. Kahn
Keyword(s):  
Dna Repair ◽  
Sinorhizobium Meliloti ◽  
Excision Repair ◽  
Uv Light ◽  
Root Hairs ◽  
Desiccation Resistance ◽  
Repair Gene ◽  
Transposon Insertion ◽  
Dna Repair Gene ◽  
Regulatory Functions

ABSTRACT Sinorhizobium meliloti can form a nitrogen-fixing symbiotic relationship with alfalfa after bacteria in the soil infect emerging root hairs of the growing plant. To be successful at this, the bacteria must be able to survive in the soil between periods of active plant growth, including when conditions are dry. The ability of S. meliloti to withstand desiccation has been known for years, but genes that contribute to this phenotype have not been identified. Transposon mutagenesis was used in combination with novel screening techniques to identify four desiccation-sensitive mutants of S. meliloti Rm1021. DNA sequencing of the transposon insertion sites identified three genes with regulatory functions (relA, rpoE2, and hpr) and a DNA repair gene (uvrC). Various phenotypes of the mutants were determined, including their behavior on several indicator media and in symbiosis. All of the mutants formed an effective symbiosis with alfalfa. To test the hypothesis that UvrC-related excision repair was important in desiccation resistance, uvrA, uvrB, and uvrC deletion mutants were also constructed. These strains were sensitive to DNA damage induced by UV light and 4-NQO and were also desiccation sensitive. These data indicate that uvr gene-mediated DNA repair and the regulation of stress-induced pathways are important for desiccation resistance.

scholarly journals Molecular cloning and chromosomal localization of DNA sequences associated with a human DNA repair gene.

1985 ◽  
Vol 5 (2) ◽  
pp. 398-405 ◽  
Author(s):  
J S Rubin ◽  
V R Prideaux ◽  
H F Willard ◽  
A M Dulhanty ◽  
G F Whitmore ◽  
...  
Keyword(s):  
Dna Repair ◽  
Dna Sequences ◽  
Chromosomal Localization ◽  
Excision Repair ◽  
Repair Process ◽  
Human Cells ◽  
Gene Products ◽  
Repair Gene ◽  
Human Dna ◽  
Dna Repair Gene

The genes and gene products involved in the mammalian DNA repair processes have yet to be identified. Toward this end we made use of a number of DNA repair-proficient transformants that were generated after transfection of DNA from repair-proficient human cells into a mutant hamster line that is defective in the initial incision step of the excision repair process. In this report, biochemical evidence is presented that demonstrates that these transformants are repair proficient. In addition, we describe the molecular identification and cloning of unique DNA sequences closely associated with the transfected human DNA repair gene and demonstrate the presence of homologous DNA sequences in human cells and in the repair-proficient DNA transformants. The chromosomal location of these sequences was determined by using a panel of rodent-human somatic cell hybrids. Both unique DNA sequences were found to be on human chromosome 19.

scholarly journals A yeast DNA repair gene partially complements defective excision repair in mammalian cells.

1988 ◽  
Vol 7 (10) ◽  
pp. 3245-3253 ◽  
Author(s):  
C. Lambert ◽  
L. B. Couto ◽  
W. A. Weiss ◽  
R. A. Schultz ◽  
L. H. Thompson ◽  
...  
Keyword(s):  
Dna Repair ◽  
Mammalian Cells ◽  
Excision Repair ◽  
Repair Gene ◽  
Dna Repair Gene

scholarly journals Repair of UV damage in plants by nucleotide excision repair: Arabidopsis UVH1 DNA repair gene is a homolog of Saccharomyces cerevisiae Rad1

2000 ◽  
Vol 21 (6) ◽  
pp. 519-528 ◽  
Author(s):  
Zongrang Liu ◽  
Gazi Showkat Hossain ◽  
Maria A. Islas-Osuna ◽  
David L. Mitchell ◽  
David W. Mount
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Repair ◽  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Uv Damage ◽  
Repair Gene ◽  
Dna Repair Gene ◽  
Nucleotide Excision

scholarly journals Allele and Genotype Distributions of DNA Repair Gene Polymorphisms in South Indian Healthy Population

2014 ◽  
Vol 6 ◽  
pp. BIC.S19681 ◽  
Author(s):  
Katiboina Srinivasa Rao ◽  
Abialbon Paul ◽  
Annan Sudarsan Arun Kumar ◽  
Gurusamy Umamaheswaran ◽  
Biswajit Dubashi ◽  
...  
Keyword(s):  
Dna Repair ◽  
Xeroderma Pigmentosum ◽  
Excision Repair ◽  
Association Studies ◽  
Healthy Population ◽  
Repair Gene ◽  
South Indian ◽  
Dna Repair Gene ◽  
Genes Encoding ◽  
Hapmap Populations

Various DNA repair pathways protect the structural and chemical integrity of the human genome from environmental and endogenous threats. Polymorphisms of genes encoding the proteins involved in DNA repair have been found to be associated with cancer risk and chemotherapeutic response. In this study, we aim to establish the normative frequencies of DNA repair genes in South Indian healthy population and compare with HapMap populations. Genotyping was done on 128 healthy volunteers from South India, and the allele and genotype distributions were established. The minor allele frequency of Xeroderma pigmentosum group A ( XPA) G23A, Excision repair cross-complementing 2 ( ERCC2)/Xeroderma pigmentosum group D ( XPD) Lys751Gln, Xeroderma pigmentosum group G ( XPG) His46His, XPG Asp1104His, and X-ray repair cross-complementing group 1 ( XRCC1) Arg399Gln polymorphisms were 49.2%, 36.3%, 48.0%, 23.0%, and 34.0% respectively. Ethnic variations were observed in the frequency distribution of these polymorphisms between the South Indians and other HapMap populations. The present work forms the groundwork for cancer association studies and biomarker identification for treatment response and prognosis.

scholarly journals DNA damage activates mTORC1 signaling in podocytes leading to glomerulosclerosis

2020 ◽  
Author(s):  
Fabian Braun ◽  
Linda Blomberg ◽  
Roman Akbar-Haase ◽  
Victor G. Puelles ◽  
Milagros N. Wong ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Kidney Disease ◽  
Excision Repair ◽  
Repair Gene ◽  
Glomerular Diseases ◽  
Genomic Stress ◽  
Dna Repair Gene ◽  
Mtorc1 Signaling

AbstractDNA repair is essential for preserving genome integrity and ensures cellular functionality and survival. Podocytes have a very limited regenerative capacity, and their survival is essential to maintain kidney function. While podocyte depletion is a hallmark of glomerular diseases, the mechanisms leading to severe podocyte injury and loss remain largely unclear. We detected perturbations in DNA repair in biopsies from patients with various podocyte-related glomerular diseases and identified single-nucleotide polymorphisms associated with the expression of DNA repair genes in patients suffering from proteinuric kidney disease. Genome maintenance through nucleotide excision repair (NER) proved to be indispensable for podocyte homeostasis. Podocyte-specific knockout of the NER endonuclease co-factor Ercc1 resulted in accumulation of DNA damage, proteinuria, podocyte loss and glomerulosclerosis. The response to this genomic stress was fundamentally different to other cell types, as podocytes activate mTORC1 signaling upon DNA damage in vitro and in vivo.Visual AbstractSchematic overview of main findings – Accumulation of genomic stress in podocytes occurs through endogenous or exogenous agents as well as genetic factors causing decreased DNA repair gene expression. Excessive DNA damage leads to the activation of mTORC1 triggering podocyte effacement, loss, glomerular scarring and proteinuric kidney disease.

scholarly journals Conserved pattern of antisense overlapping transcription in the homologous human ERCC-1 and yeast RAD10 DNA repair gene regions.

1989 ◽  
Vol 9 (4) ◽  
pp. 1794-1798 ◽  
Author(s):  
M van Duin ◽  
J van Den Tol ◽  
J H Hoeijmakers ◽  
D Bootsma ◽  
I P Rupp ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Repair ◽  
Excision Repair ◽  
Antisense Transcription ◽  
Human Cells ◽  
Repair Gene ◽  
Naturally Occurring ◽  
Dna Repair Gene ◽  
Evolutionarily Conserved ◽  
Overlapping Transcription

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.

scholarly journals Histone deacetylase SIRT1 modulates and deacetylates DNA base excision repair enzyme thymine DNA glycosylase

2013 ◽  
Vol 456 (1) ◽  
pp. 89-98 ◽  
Author(s):  
Amrita Madabushi ◽  
Bor-Jang Hwang ◽  
Jin Jin ◽  
A-Lien Lu
Keyword(s):  
Dna Repair ◽  
Histone Deacetylase ◽  
Excision Repair ◽  
Dna Glycosylase ◽  
Repair Enzyme ◽  
Repair Gene ◽  
Thymine Dna Glycosylase ◽  
Dna Base Excision Repair ◽  
Dna Repair Gene ◽  
Base Excision

SIRT1 histone deacetylase interacts with the DNA repair enzyme thymine DNA glycosylase (TDG). SIRT1 inhibits TDG expression and deacetylates TDG to modulate TDG activity and substrate specificity. These interactions may mediate DNA repair, gene expression and drug cytotoxicity.

scholarly journals DNA Repair Gene Polymorphisms and Chromosomal Aberrations in Exposed Populations

2021 ◽  
Vol 12 ◽  
Author(s):  
Yasmeen Niazi ◽  
Hauke Thomsen ◽  
Bozena Smolkova ◽  
Ludmila Vodickova ◽  
Sona Vodenkova ◽  
...  
Keyword(s):  
Dna Repair ◽  
Chromosomal Aberrations ◽  
Gene Polymorphisms ◽  
Excision Repair ◽  
Association Studies ◽  
Peripheral Blood Lymphocytes ◽  
Mismatch Repair Gene ◽  
Genome Wide Association Studies ◽  
Repair Gene ◽  
Dna Repair Gene

DNA damage and unrepaired or insufficiently repaired DNA double-strand breaks as well as telomere shortening contribute to the formation of structural chromosomal aberrations (CAs). Non-specific CAs have been used in the monitoring of individuals exposed to potential carcinogenic chemicals and radiation. The frequency of CAs in peripheral blood lymphocytes (PBLs) has been associated with cancer risk and the association has also been found in incident cancer patients. CAs include chromosome-type aberrations (CSAs) and chromatid-type aberrations (CTAs) and their sum CAtot. In the present study, we used data from our published genome-wide association studies (GWASs) and extracted the results for 153 DNA repair genes for 607 persons who had occupational exposure to diverse harmful substances/radiation and/or personal exposure to tobacco smoking. The analyses were conducted using linear and logistic regression models to study the association of DNA repair gene polymorphisms with CAs. Considering an arbitrary cutoff level of 5 × 10–3, 14 loci passed the threshold, and included 7 repair pathways for CTA, 4 for CSA, and 3 for CAtot; 10 SNPs were eQTLs influencing the expression of the target repair gene. For the base excision repair pathway, the implicated genes PARP1 and PARP2 encode poly(ADP-ribosyl) transferases with multiple regulatory functions. PARP1 and PARP2 have an important role in maintaining genome stability through diverse mechanisms. Other candidate genes with known roles for CSAs included GTF2H (general transcription factor IIH subunits 4 and 5), Fanconi anemia pathway genes, and PMS2, a mismatch repair gene. The present results suggest pathways with mechanistic rationale for the formation of CAs and emphasize the need to further develop techniques for measuring individual sensitivity to genotoxic exposure.

The Saccharomyces cerevisiae DNA repair gene RAD23 encodes a nuclear protein containing a ubiquitin-like domain required for biological function

1993 ◽  
Vol 13 (12) ◽  
pp. 7757-7765
Author(s):  
J F Watkins ◽  
P Sung ◽  
L Prakash ◽  
S Prakash
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Repair ◽  
Protein Function ◽  
Nuclear Protein ◽  
Biological Function ◽  
Excision Repair ◽  
Cellular Proteins ◽  
Repair Gene ◽  
Dna Repair Gene

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.

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