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The system involves the RecA protein (Rad51 in eukaryotes). The RecA protein, stimulated by single-stranded DNA, is involved in the inactivation of the repressor of SOS response genes thereby inducing the response. It is an error-prone repair system that contributes significantly to DNA changes observed in a wide range of species.
XthA (exonuclease III, a DNA repair enzyme) and KatE (catalase) are known to play important roles in the defense against oxidative stress but KatF regulon genes are not induced by oxidative stress. [2] There is an overlap between oxidative stress response and other regulatory networks like heat shock response, SOS response.
Epigenetic alterations can accompany DNA repair of oxidative damage or double-strand breaks. In human cells, oxidative DNA damage occurs about 10,000 times a day and DNA double-strand breaks occur about 10 to 50 times a cell cycle in somatic replicating cells (see DNA damage (naturally occurring)). The selective advantage of DNA repair is to ...
More than 100 types of oxidative DNA damage have been characterized, and 8-oxodG constitutes about 5% of the steady state oxidative damages in DNA. [18] Helbock et al. [ 14 ] estimated that there were 24,000 steady state oxidative DNA adducts per cell in young rats and 66,000 adducts per cell in old rats.
It is involved in oxidative DNA damage repair and is part of the base excision repair pathway. The enzyme excises adenine bases from the DNA backbone at sites where adenine is inappropriately paired with guanine, cytosine, or 8-oxo-7,8-dihydroguanine, a common form of oxidative DNA damage. The protein is localized to the nucleus and mitochondria.
In DNA repair, the Fe (II)/2-oxoglutarate-dependent dioxygenase AlkB, functions in the oxidative removal of alkylation damage to DNA. Failure to remove DNA alkylation damage can result in cytotoxicity or mutagenesis during DNA replication.
Mycobacterium smegmatis relies on DNA repair pathways to resist DNA damage. Double-strand breaks are especially threatening to bacterial viability. M. smegmatis has three options for repairing double-strand breaks; homologous recombination (HR), non-homologous end joining (NHEJ), and single-strand annealing (SSA). [16]
Many genes under RpoS control confer stress resistance to assaults such as DNA damage, presence of reactive oxygen species and osmotic shock. The product of xthA is an exonuclease that participates in DNA repair by recognizing and removing 5’ monophosphates near abasic sites in damaged DNA. [12]