scholarly journals Base excision repair in sugarcane

2001 ◽  
Vol 24 (1-4) ◽  
pp. 123-129 ◽  
Author(s):  
Lucymara F. Agnez-Lima ◽  
Sílvia R. Batistuzzo de Medeiros ◽  
Bruno S. Maggi ◽  
Giovanna A.S. Quaresma
Keyword(s):  
Dna Repair ◽  
Base Excision Repair ◽  
Expressed Sequence Tag ◽  
Excision Repair ◽  
Low Frequency ◽  
Cellular Processes ◽  
Base Excision ◽  
Mining Work ◽  
Physical And Chemical ◽  
Repair Genes

DNA damage can be induced by a large number of physical and chemical agents from the environment as well as compounds produced by cellular metabolism. This type of damage can interfere with cellular processes such as replication and transcription, resulting in cell death and/or mutations. The low frequency of mutagenesis in cells is due to the presence of enzymatic pathways which repair damaged DNA. Several DNA repair genes (mainly from bacteria, yeasts and mammals) have been cloned and their products characterized. The high conservation, especially in eukaryotes, of the majority of genes related to DNA repair argues for their importance in the maintenance of life on earth. In plants, our understanding of DNA repair pathways is still very poor, the first plant repair genes having only been cloned in 1997 and the mechanisms of their products have not yet been characterized. The objective of our data mining work was to identify genes related to the base excision repair (BER) pathway, which are present in the database of the Sugarcane Expressed Sequence Tag (SUCEST) Project. This search was performed by tblastn program. We identified sugarcane clusters homologous to the majority of BER proteins used in the analysis and a high degree of conservation was observed. The best results were obtained with BER proteins from Arabidopsis thaliana. For some sugarcane BER genes, the presence of more than one form of mRNA is possible, as shown by the occurrence of more than one homologous EST cluster.

Incorporation of 5’,8-cyclo-2’deoxyadenosines by DNA repair polymerases via base excision repair

DNA Repair ◽  
2021 ◽  
pp. 103258
Author(s):  
Pawlos S. Tsegay ◽  
Daniela Hernandez ◽  
Christopher Brache ◽  
Chryssostomos Chatgilialoglu ◽  
Marios G. Krokidis ◽  
...  
Keyword(s):  
Dna Repair ◽  
Base Excision Repair ◽  
Excision Repair ◽  
Base Excision

scholarly journals Expansion of base excision repair compensates for a lack of DNA repair by oxidative dealkylation in budding yeast

2019 ◽  
Vol 294 (37) ◽  
pp. 13629-13637 ◽  
Author(s):  
Suzanne J. Admiraal ◽  
Daniel E. Eyler ◽  
Michael R. Baldwin ◽  
Emily M. Brines ◽  
Christopher T. Lohans ◽  
...  
Keyword(s):  
Dna Repair ◽  
Base Excision Repair ◽  
Excision Repair ◽  
Budding Yeast ◽  
Base Excision

scholarly journals Impact of hypoxia on DNA repair and genome integrity

Mutagenesis ◽  
2019 ◽  
Vol 35 (1) ◽  
pp. 61-68 ◽  
Author(s):  
Alanna R Kaplan ◽  
Peter M Glazer
Keyword(s):  
Dna Repair ◽  
Cancer Progression ◽  
Base Excision Repair ◽  
Mutation Frequency ◽  
Excision Repair ◽  
Tumour Microenvironment ◽  
Genome Integrity ◽  
Future Directions ◽  
Homology Directed Repair ◽  
Base Excision

Abstract Hypoxia is a hallmark of the tumour microenvironment with profound effects on tumour biology, influencing cancer progression, the development of metastasis and patient outcome. Hypoxia also contributes to genomic instability and mutation frequency by inhibiting DNA repair pathways. This review summarises the diverse mechanisms by which hypoxia affects DNA repair, including suppression of homology-directed repair, mismatch repair and base excision repair. We also discuss the effects of hypoxia mimetics and agents that induce hypoxia on DNA repair, and we highlight areas of potential clinical relevance as well as future directions.

scholarly journals Dynamic Compartmentalization of Base Excision Repair Proteins in Response to Nuclear and Mitochondrial Oxidative Stress

2008 ◽  
Vol 29 (3) ◽  
pp. 794-807 ◽  
Author(s):  
Lyra M. Griffiths ◽  
Dan Swartzlander ◽  
Kellen L. Meadows ◽  
Keith D. Wilkinson ◽  
Anita H. Corbett ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Dna Repair ◽  
Base Excision Repair ◽  
Oxidative Dna Damage ◽  
Excision Repair ◽  
Intracellular Localization ◽  
Genotoxic Stress ◽  
Mitochondrial Oxidative Stress ◽  
Base Excision

ABSTRACT DNAs harbored in both nuclei and mitochondria of eukaryotic cells are subject to continuous oxidative damage resulting from normal metabolic activities or environmental insults. Oxidative DNA damage is primarily reversed by the base excision repair (BER) pathway, initiated by N-glycosylase apurinic/apyrimidinic (AP) lyase proteins. To execute an appropriate repair response, BER components must be distributed to accommodate levels of genotoxic stress that may vary considerably between nuclei and mitochondria, depending on the growth state and stress environment of the cell. Numerous examples exist where cells respond to signals, resulting in relocalization of proteins involved in key biological transactions. To address whether such dynamic localization contributes to efficient organelle-specific DNA repair, we determined the intracellular localization of the Saccharomyces cerevisiae N-glycosylase/AP lyases, Ntg1 and Ntg2, in response to nuclear and mitochondrial oxidative stress. Fluorescence microscopy revealed that Ntg1 is differentially localized to nuclei and mitochondria, likely in response to the oxidative DNA damage status of the organelle. Sumoylation is associated with targeting of Ntg1 to nuclei containing oxidative DNA damage. These studies demonstrate that trafficking of DNA repair proteins to organelles containing high levels of oxidative DNA damage may be a central point for regulating BER in response to oxidative stress.

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