To fix depurination and deamination, base excision repair is used. In BER, glylocalyse flips out the wrong base and cuts it off. It is called apurinic or apyrimidinic once the base has been cut out. Next, AP endonuclease cuts the sugar and the phosphate out. DNA polymerase and ligase put in the new nucleotide and seal the gap. Thymine dimers, which are covalently linked and distort the helix, are created by UV radiation. This is a bulky distortion in the DNA and DNA polymerase cannot make it through. Some special DNA polymerases can replicate using this damaged DNA, but they are error prone and not used often. Thymine dimers are fixed by nucleotide excision repair. In NER, the nuclease cleaves around the bulky lesion. Helicase is required to pull apart the DNA, but it is a specialized helicase. Clamps are needed for BER & NER to recruit proteins and active the excision.
Xeroderma Pigmentosum is a rare recessive disorder, where UV damage cannot be repaired in the DNA through NER. Skin lesions and skin cancer occur from the sun.
Double strand breaks in the DNA result in cancer, premature again, apoptosis and chromosome reengagement. The cell does do breakage on purpose during recombination and VDJ. To fix accidental breakage, non-homologous end joining and homologous rearrangement are used. Non-homologous ending joining happens by nucleases come in and create blunt ends and remove several bases and seals back together. Loss of genetic information occurs but it is very commonly used in cells during G1. Homologous rearrangement requires for a separate piece of DNA that the matches the broken on exactly. The DNA is completely repaired. The 3’ end overhangs and invades the other strand that looks like the damaged DNA and base pairs. DNA polymerase synthesized across the area using the other strand as template. Ligase fixes the nick. This repair occurs in s phase, g2 phase, m phase. Basically when another copy of the DNA is present.