scholarly journals Altitudinal Heterogeneity of UV Adaptation in Phytophthorainfestans Is Associated with the Spatial Distribution of a DNA Repair Gene

2021 ◽  
Vol 7 (4) ◽  
pp. 245
Author(s):  
Yan-Ping Wang ◽  
Abdul Waheed ◽  
Shi-Ting Liu ◽  
Wen-Yang Li ◽  
Oswald Nkurikiyimfura ◽  
...  
Keyword(s):  
Climate Change ◽  
Uv Irradiation ◽  
Climatic Factors ◽  
Excision Repair ◽  
Natural Ecosystems ◽  
Repair Gene ◽  
Dna Repair Gene ◽  
Uv Tolerance ◽  
Specific Variation ◽  
Late Blight Pathogen

Climate change is considered a major threat to society and nature. UV irradiation is the most important environmental genotoxic agent. Thus, how elevated UV irradiation may influence human health and ecosystems has generated wide concern in the scientific community, as well as with policy makers and the public in general. In this study, we investigated patterns and mechanisms of UV adaptation in natural ecosystems by studying a gene-specific variation in the potato late blight pathogen, Phytophthora infestans. We compared the sequence characteristics of radiation sensitive 23 (RAD23), a gene involved in the nucleotide excision repair (NER) pathway and UV tolerance, in P. infestans isolates sampled from various altitudes. We found that lower genetic variation in the RAD23 gene was caused by natural selection. The hypothesis that UV irradiation drives this selection was supported by strong correlations between the genomic characteristics and altitudinal origin (historic UV irradiation) of the RAD23 sequences with UV tolerance of the P. infestans isolates. These results indicate that the RAD23 gene plays an important role in the adaptation of P. infestans to UV stress. We also found that different climatic factors could work synergistically to determine the evolutionary adaptation of species, making the influence of climate change on ecological functions and resilience more difficult to predict. Future attention should aim at understanding the collective impact generated by simultaneous change in several climate factors on species adaptation and ecological sustainability, using state of the art technologies such as experimental evolution, genome-wide scanning, and proteomics.

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 Developmental Defects and Male Sterility in Mice Lacking the Ubiquitin-Like DNA Repair Gene mHR23B

2002 ◽  
Vol 22 (4) ◽  
pp. 1233-1245 ◽  
Author(s):  
Jessica M. Y. Ng ◽  
Harry Vrieling ◽  
Kaoru Sugasawa ◽  
Marja P. Ooms ◽  
J. Anton Grootegoed ◽  
...  
Keyword(s):  
Male Sterility ◽  
Excision Repair ◽  
High Rate ◽  
Repair Gene ◽  
Developmental Defects ◽  
Mouse Mutants ◽  
Dna Repair Gene ◽  
Ubiquitin Proteasome ◽  
In Vitro Repair

ABSTRACT mHR23B encodes one of the two mammalian homologs of Saccharomyces cerevisiae RAD23, a ubiquitin-like fusion protein involved in nucleotide excision repair (NER). Part of mHR23B is complexed with the XPC protein, and this heterodimer functions as the main damage detector and initiator of global genome NER. While XPC defects exist in humans and mice, mutations for mHR23A and mHR23B are not known. Here, we present a mouse model for mHR23B. Unlike XPC-deficient cells, mHR23B−/− mouse embryonic fibroblasts are not UV sensitive and retain the repair characteristics of wild-type cells. In agreement with the results of in vitro repair studies, this indicates that mHR23A can functionally replace mHR23B in NER. Unexpectedly, mHR23B−/− mice show impaired embryonic development and a high rate (90%) of intrauterine or neonatal death. Surviving animals display a variety of abnormalities, including retarded growth, facial dysmorphology, and male sterility. Such abnormalities are not observed in XPC and other NER-deficient mouse mutants and point to a separate function of mHR23B in development. This function may involve regulation of protein stability via the ubiquitin/proteasome pathway and is not or only in part compensated for by mHR23A.

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.

ERCC-1 (E) expression and its effect on survival in patients (pts) receiving concurrent cisplatin (C) and radiation (R) for locally advanced head and neck cancer (HNC)

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e17033-e17033
Author(s):  
C. T. Lan ◽  
R. H. Amirkhan ◽  
T. Gray ◽  
Y. Xie ◽  
J. E. Dowell
Keyword(s):  
Excision Repair ◽  
Performance Status ◽  
Univariate Analysis ◽  
Locally Advanced ◽  
Stage Iv ◽  
Tumor Grade ◽  
Medical Systems ◽  
Significant Independent Predictor ◽  
Repair Gene ◽  
Dna Repair Gene

e17033 Background: E is a DNA repair gene involved in the nucleotide excision repair pathway. Overexpression of E has been associated with resistance to C in patients with ovarian, gastric, and lung cancer. We retrospectively analyzed tissue from HNC pts who received concurrent C and R to determine if E expression was a significant independent predictor of survival. Methods: Eligible HNC pts had squamous cell histology and received definitive concurrent C and R at the Dallas VAMC. Tissue was immunostained for E using ERCC-1,clone 8F, 1:100 dilution (Abcam, Cat#ab2356, Cambridge, MA) diluted in ChemMate buffer (Ventana Medical Systems, Tucson, AZ) on a BenchMarkXT automated immunostainer using the UltraVIEW system with horseradish peroxidase and diaminobenzidine (DAB) chromogen (Ventana Medical Systems, Tucson, AZ) per the standard protocol of the UT Southwestern Pathology Immunohistochemistry Laboratory. E scoring was determined by 2 pathologists blinded to clinical outcomes. Scoring was as follows: 0 = 0% of tumor nuclei were positive, 1+ = less than 50%, 2+ = 50–75% and 3+ = 75–100%. Results: 73 consecutively treated patients were analyzed. Median age 59 (range 41 - 80); 99% male; 7% stage II, 19% stage III, 73% stage IV; primary site - 4% oral cavity, 56% oropharynx, 14% hypopharynx, 23% larynx, 3% nasopharynx; Tumor grade - 60% moderately differentiated, 4% well differentiated, 15% poorly differentiated, 21% not specified; Performance status 0–25%, 1–45%, 2–8%, unknown-22%; E scoring was 0 in 0%, 1+ (14%), 2+ (42%), 3+ (44%). In univariate analysis, E staining 3+ was not predictive of survival with a hazard ratio (HR) of .796 (95% CI .44–1.43; p = 0.44). In multivariate analysis, the only significant predictor was hypopharynx with a HR of 3.18 (95% CI 1.02–9.88; p = 0.046). HR for age > 60 was 2.16 (95% CI .96–4.86; p = 0.06). E staining 3+ was not predictive of survival with a HR of .69 (95% CI .3–1.56; p = 0.37). Median survival (MS) for the whole group was 2.8 years (y); 5y survival - 41%. MS for the E 3+ pts - 2.1y; 5y survival 38%. MS for the E < 3+ pts - 2.9y; 5y survival 44% (p = not significant). Conclusions: In our retrospective review of HNC patients receiving concurrent C and R, E staining was not a significant predictor of survival. No significant financial relationships to disclose.

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