34 Facts About DNA repair

DNA repair is a collection of processes by which a cell identifies and corrects damage to the DNA molecules that encode its genome.

In human cells, both normal metabolic activities and environmental factors such as radiation can cause DNA repair damage, resulting in tens of thousands of individual molecular lesions per cell per day.

Rate of DNA repair is dependent on many factors, including the cell type, the age of the cell, and the extracellular environment.

Unlike proteins and RNA, DNA repair usually lacks tertiary structure and therefore damage or disturbance does not occur at that level.

DNA repair is supercoiled and wound around "packaging" proteins called histones, and both superstructures are vulnerable to the effects of DNA repair damage.

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Constitutive DNA repair damage caused by endogenous oxidants can be detected as a low level of histone H2AX phosphorylation in untreated cells.

Nuclear DNA repair exists as chromatin during non-replicative stages of the cell cycle and is condensed into aggregate structures known as chromosomes during cell division.

In either state the DNA repair is highly compacted and wound up around bead-like proteins called histones.

Whenever a cell needs to express the genetic information encoded in its nDNA repair the required chromosomal region is unravelled, genes located therein are expressed, and then the region is condensed back to its resting conformation.

Mitochondrial DNA repair is located inside mitochondria organelles, exists in multiple copies, and is tightly associated with a number of proteins to form a complex known as the nucleoid.

In contrast to DNA repair damage, a mutation is a change in the base sequence of the DNA repair.

Once damage is localized, specific DNA repair molecules bind at or near the site of damage, inducing other molecules to bind and form a complex that enables the actual repair to take place.

The third type of DNA repair damage reversed by cells is certain methylation of the bases cytosine and adenine.

The enzymatic machinery responsible for this DNA repair process is nearly identical to the machinery responsible for chromosomal crossover during meiosis.

Viability was very low in a strain lacking pol II, pol IV, and pol V, the three SOS-inducible DNA repair polymerases, indicating that translesion synthesis is conducted primarily by these specialized DNA repair polymerases.

DNA repair damage checkpoint is a signal transduction pathway that blocks cell cycle progression in G1, G2 and metaphase and slows down the rate of S phase progression when DNA repair is damaged.

Central to all DNA repair damage induced checkpoints responses is a pair of large protein kinases belonging to the first group of PI3K-like protein kinases-the ATM and ATR kinases, whose sequence and functions have been well conserved in evolution.

RecA–ssDNA repair filaments activate LexA autoprotease activity, which ultimately leads to cleavage of LexA dimer and subsequent LexA degradation.

The lesion DNA repair genes are induced at the beginning of SOS response.

Once the DNA damage is repaired or bypassed using polymerases or through recombination, the amount of single-stranded DNA in cells is decreased, lowering the amounts of RecA filaments decreases cleavage activity of LexA homodimer, which then binds to the SOS boxes near promoters and restores normal gene expression.

Exposure of yeast Saccharomyces cerevisiae to DNA repair damaging agents results in overlapping but distinct transcriptional profiles.

In general global response to DNA damage involves expression of multiple genes responsible for postreplication repair, homologous recombination, nucleotide excision repair, DNA damage checkpoint, global transcriptional activation, genes controlling mRNA decay, and many others.

Experimental animals with genetic deficiencies in DNA repair often show decreased life span and increased cancer incidence.

In similar manner, mice deficient in a key repair and transcription protein that unwinds DNA helices have premature onset of aging-related diseases and consequent shortening of lifespan.

However, not every DNA repair deficiency creates exactly the predicted effects; mice deficient in the NER pathway exhibited shortened life span without correspondingly higher rates of mutation.

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The molecular mechanisms by which such restriction results in lengthened lifespan are as yet unclear ; however, the behavior of many genes known to be involved in DNA repair is altered under conditions of caloric restriction.

Several agents reported to have anti-aging properties have been shown to attenuate constitutive level of mTOR signaling, an evidence of reduction of metabolic activity, and concurrently to reduce constitutive level of DNA repair damage induced by endogenously generated reactive oxygen species.

The mammalian homolog of SIR-2 is known to induce downstream DNA repair factors involved in NHEJ, an activity that is especially promoted under conditions of caloric restriction.

Tumor cells with partial loss of DNA damage response are dependent on another mechanism – single-strand break repair – which is a mechanism consisting, in part, of the PARP1 gene product.

Tumor cells relying on this residual DNA repair mechanism are unable to repair the damage and hence are not able to survive and proliferate, whereas normal cells can repair the damage with the functioning homologous recombination mechanism.

In experimental mouse models, loss of DNA repair damage response-mediated cell senescence was observed after using a short hairpin RNA to inhibit the double-strand break response kinase ataxia telangiectasia, leading to increased tumor size and invasiveness.

When DNA repair is deficient DNA damages remain in cells at a higher than usual level and these excess damages cause increased frequencies of mutation or epimutation.

Basic processes of DNA repair are highly conserved among both prokaryotes and eukaryotes and even among bacteriophages ; however, more complex organisms with more complex genomes have correspondingly more complex repair mechanisms.

On some occasions, DNA damage is not repaired or is repaired by an error-prone mechanism that results in a change from the original sequence.