Base Excision Repair | DNA Repair Mechanism 

The Base excision repair (BER) is a cellular mechanism that repairs damaged DNA throughout the cell cycle. It is responsible primarily for removing small, non-helix-distorting base lesions from the genome. The related nucleotide excision repair pathway repairs bulky helix-distorting lesions. BER is important for removing damaged bases that could otherwise cause mutations by mispairing or lead to breaks in DNA during replication. BER is initiated by DNA glycosylases, which recognize and remove specific damaged or inappropriate bases, forming AP sites. These are then cleaved by an AP endonuclease. The resulting single-strand break can then be processed by either short-patch (where a single nucleotide is replaced) or long-patch BER .
The Base Excision repair mechanism makes use of the following enzymes to repair the DNA :
DNA Glycosylase
AP Endonuclease
DNA Polymerase
DNA Ligase
The Base Excision Repair , is initiated by the damaged DNA due to chemicals and radiations.The Base Excision repair is a single strand repair mechanism where single base gets transformed into different base like in Hydrolytic Deamination where Cytosine changes into Uracil thereby changing the genetic code.
Single bases in DNA can be chemically damaged by a variety of mechanisms, the most common ones being deamination, oxidation, and alkylation. These modifications can affect the ability of the base to hydrogen-bond, resulting in incorrect base-pairing, and, as a consequence, mutations in the DNA. For example, incorporation of adenine across from 8-oxoguanine (right) during DNA replication causes a G:C base pair to be mutated to T:A. Other examples of base lesions repaired by BER include:
Oxidized bases: 8-oxoguanine, 2,6-diamino-4-hydroxy-5-formamidopyrimidine (FapyG, FapyA)
Alkylated bases: 3-methyladenine, 7-methylguanosine
Deaminated bases: hypoxanthine formed from deamination of adenine. Xanthine formed from deamination of guanine. (Thymidine products following deamination of 5-methylcytosine are more difficult to recognize, but can be repaired by mismatch-specific glycosylases)
Uracil inappropriately incorporated in DNA or formed by deamination of cytosine[2]
In addition to base lesions, the downstream steps of BER are also utilized to repair single-strand breaks.