scholarly journals Investigating the role of DNA repair enzymes in DNA replication and recombination (735.3)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Clayton Speed ◽  
Claudia Wiese ◽  
Ann Parplys ◽  
J. Robert Hatherill
Keyword(s):  
Dna Repair ◽  
Dna Replication ◽  
Dna Repair Enzymes ◽  
Repair Enzymes

scholarly journals Maladaptive DNA repair is the ultimate contributor to the death of trimethoprim-treated cells under aerobic and anaerobic conditions

2017 ◽  
Vol 114 (43) ◽  
pp. 11512-11517 ◽  
Author(s):  
Xavier Giroux ◽  
Wei-Lin Su ◽  
Marie-Florence Bredeche ◽  
Ivan Matic
Keyword(s):  
Cell Death ◽  
Dna Repair ◽  
Dna Replication ◽  
Dna Lesions ◽  
Replication Initiation ◽  
Anaerobic Conditions ◽  
Dna Repair Enzymes ◽  
Repair Enzymes ◽  
Aerobic And Anaerobic ◽  
Aerobic And Anaerobic Conditions

The bactericidal effects of antibiotics are undoubtedly triggered by target-specific interactions, but there is growing evidence that an important aspect of cytotoxicity results from treatment-induced metabolic perturbations. In this study, we characterized molecular mechanisms whereby trimethoprim treatment results in cell death, usingEscherichia colias the model organism.E. colicells grown in rich medium that contained all amino acids and low amounts of thymidine were treated with trimethoprim under aerobic and anaerobic conditions. Under these growth conditions, accelerated thymine depletion is the primary trigger of the processes leading to cell death. Thymine depletion-induced DNA replication stress leads to the production of reactive oxygen species under aerobic conditions and of the DNA-damaging byproducts of nitrate respiration under anaerobic conditions. Lowering the DNA replication initiation rate by introducing thednaA(Sx) allele or by overexpressing Hda protein reduces the number of active replication forks, which reduces the consumption of thymidine and increases resistance to trimethoprim under both aerobic and anaerobic conditions. Analysis of the involvement of DNA repair enzymes in trimethoprim-induced cytotoxicity clearly indicates that different amounts and/or different types of DNA lesions are produced in the presence or absence of oxygen. Maladaptive processing of the DNA damage by DNA repair enzymes, in particular by MutM and MutY DNA glycosylases, ultimately contributes to cell death.

scholarly journals DASH-type cryptochromes – solved and open questions

2020 ◽  
Vol 401 (12) ◽  
pp. 1487-1493
Author(s):  
Stephan Kiontke ◽  
Tanja Göbel ◽  
Annika Brych ◽  
Alfred Batschauer
Keyword(s):  
Dna Repair ◽  
Circadian Clock ◽  
Blue Light ◽  
Dna Repair Enzymes ◽  
Repair Enzymes ◽  
Open Questions ◽  
Essential Components ◽  
Repair Activity ◽  
Almost All ◽  
Uv Lesions

AbstractDrosophila, Arabidopsis, Synechocystis, human (DASH)-type cryptochromes (cry-DASHs) form one subclade of the cryptochrome/photolyase family (CPF). CPF members are flavoproteins that act as DNA-repair enzymes (DNA-photolyases), or as ultraviolet(UV)-A/blue light photoreceptors (cryptochromes). In mammals, cryptochromes are essential components of the circadian clock feed-back loop. Cry-DASHs are present in almost all major taxa and were initially considered as photoreceptors. Later studies demonstrated DNA-repair activity that was, however, restricted to UV-lesions in single-stranded DNA. Very recent studies, particularly on microbial organisms, substantiated photoreceptor functions of cry-DASHs suggesting that they could be transitions between photolyases and cryptochromes.

Role of yeast Rth1 nuclease and its homologs in mutation avoidance, DNA repair, and DNA replication

1998 ◽  
Vol 34 (1) ◽  
pp. 21-29 ◽  
Author(s):  
Robert E. Johnson ◽  
Gopala K. Kovvali ◽  
Louise Prakash ◽  
S. Prakash
Keyword(s):  
Dna Repair ◽  
Dna Replication ◽  
Mutation Avoidance

DNA Repair Enzymes in Mammalian Cells

1977 ◽  
pp. 263-322 ◽  
Author(s):  
Errol C. Friedberg ◽  
Kern H. Cook ◽  
James Duncan ◽  
Kristien Mortelmans
Keyword(s):  
Dna Repair ◽  
Mammalian Cells ◽  
Dna Repair Enzymes ◽  
Repair Enzymes

scholarly journals DNA damage shifts circadian clock time via Hausp-dependent Cry1 stabilization

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Stephanie J Papp ◽  
Anne-Laure Huber ◽  
Sabine D Jordan ◽  
Anna Kriebs ◽  
Madelena Nguyen ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Circadian Clock ◽  
Transcriptional Response ◽  
Genotoxic Stress ◽  
Genomic Integrity ◽  
Clock Time ◽  
Dna Repair Enzymes ◽  
Repair Enzymes ◽  
Specific Protease

The circadian transcriptional repressors cryptochrome 1 (Cry1) and 2 (Cry2) evolved from photolyases, bacterial light-activated DNA repair enzymes. In this study, we report that while they have lost DNA repair activity, Cry1/2 adapted to protect genomic integrity by responding to DNA damage through posttranslational modification and coordinating the downstream transcriptional response. We demonstrate that genotoxic stress stimulates Cry1 phosphorylation and its deubiquitination by Herpes virus associated ubiquitin-specific protease (Hausp, a.k.a Usp7), stabilizing Cry1 and shifting circadian clock time. DNA damage also increases Cry2 interaction with Fbxl3, destabilizing Cry2. Thus, genotoxic stress increases the Cry1/Cry2 ratio, suggesting distinct functions for Cry1 and Cry2 following DNA damage. Indeed, the transcriptional response to genotoxic stress is enhanced in Cry1−/− and blunted in Cry2−/− cells. Furthermore, Cry2−/− cells accumulate damaged DNA. These results suggest that Cry1 and Cry2, which evolved from DNA repair enzymes, protect genomic integrity via coordinated transcriptional regulation.

scholarly journals Structural and cellular analyses of cancer-associated mutations in DNA repair enzymes

2019 ◽  
Vol 75 (a1) ◽  
pp. a327-a327
Author(s):  
Brian E. Eckenroth ◽  
Ash Prakash ◽  
Brittany L. Carroll ◽  
Joann B. Sweasy ◽  
Sylvie Doublié
Keyword(s):  
Dna Repair ◽  
Dna Repair Enzymes ◽  
Repair Enzymes
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