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The DNA repair ability of a cell is vital to the integrity of its genome and thus to the normal functionality of that organism. Many genes that were initially shown to influence life span have turned out to be involved in DNA damage repair and protection. [3] Paul Modrich talks about himself and his work in DNA repair.
Melanoma cells are commonly defective in postreplication repair of DNA damages that are in the form of cyclobutane pyrimidine dimers, a type of damage caused by ultraviolet radiation. [11] [12] A particular repair process that appears to be defective in melanoma cells is homologous recombinational repair. [12]
Inefficient repair of DNA damaged by ionizing radiation or chemical agents in these mutants revealed proteins essential in this pathway. Early signaling proteins in the checkpoint pathway are members of a family of phosphatidylinositol 3-kinases, rad3 in yeast and ATR in vertebrates, that are believed to localize to sites of DNA damage. [7]
Nucleotide excision repair is a DNA repair mechanism. [2] DNA damage occurs constantly because of chemicals (e.g. intercalating agents), radiation and other mutagens. Three excision repair pathways exist to repair single stranded DNA damage: Nucleotide excision repair (NER), base excision repair (BER), and DNA mismatch repair (MMR).
For instance, rad52 cells, which cannot repair double-stranded DNA breaks, tend to permanently arrest in G2 when exposed to even very low levels of x-irradiation, and rarely end up progressing through the later stages of the cell cycle. This is because the cells cannot repair DNA damage and thus do not enter mitosis.
Homology-directed repair (HDR) is a mechanism in cells to repair double-strand DNA lesions. [1] The most common form of HDR is homologous recombination . The HDR mechanism can only be used by the cell when there is a homologous piece of DNA present in the nucleus , mostly in G2 and S phase of the cell cycle .
The HRR pathway requires that a second homologous chromosome be available to allow recovery of the information lost by the first chromosome due to the double-strand damage. DNA damage appears to play a key role in mammalian aging, and an adequate level of DNA repair promotes longevity (see DNA damage theory of aging and reference. [28]).
Apurinic/apyrimidinic (AP) endonuclease is an enzyme that is involved in the DNA base excision repair pathway (BER). Its main role in the repair of damaged or mismatched nucleotides in DNA is to create a nick in the phosphodiester backbone of the AP site created when DNA glycosylase removes the damaged base.