31 Facts About DNA damage

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

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

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

Spontaneous DNA damage can include the loss of a base, deamination, sugar ring puckering and tautomeric shift.

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

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Nuclear DNA damage 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 damage 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 damage the required chromosomal region is unravelled, genes located therein are expressed, and then the region is condensed back to its resting conformation.

Mitochondrial DNA damage 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.

DNA damage can be recognized by enzymes, and thus can be correctly repaired if redundant information, such as the undamaged sequence in the complementary DNA strand or in a homologous chromosome, is available for copying.

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

Such direct reversal mechanisms are specific to the type of DNA damage incurred and do not involve breakage of the phosphodiester backbone.

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

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

The global response to DNA damage is an act directed toward the cells' own preservation and triggers multiple pathways of macromolecular repair, lesion bypass, tolerance, or apoptosis.

DNA 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 is damaged.

Central to all DNA 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 damage filaments activate LexA autoprotease activity, which ultimately leads to cleavage of LexA dimer and subsequent LexA degradation.

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.

Eukaryotic cells exposed to DNA damage damaging agents activate important defensive pathways by inducing multiple proteins involved in DNA damage repair, cell cycle checkpoint control, protein trafficking and degradation.

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

In contrast, different human cell types respond to DNA damage differently indicating an absence of a common global response.

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.

Yeast Rev1 and human polymerase ? are members of Y family translesion DNA polymerases present during global response to DNA damage and are responsible for enhanced mutagenesis during a global response to DNA damage in eukaryotes.

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

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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 damage 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 damage induced by endogenously generated reactive oxygen species.

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.

In experimental mouse models, loss of DNA 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.

Basic processes of DNA damage 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.