Base Excision Repair Targets Uracil Residues
The Base Excision Repair (BER) pathway is a crucial cellular mechanism designed to correct specific types of DNA damage.
- BER primarily targets non-helix distorting DNA lesions.
- These lesions often involve modified or incorrectly incorporated bases.
- A common substrate for BER is Uracil (U).
Uracil Removal in DNA
Uracil can arise in DNA through two main routes:
- Cytosine deamination: Cytosine (C) can spontaneously deaminate to form Uracil (U). If not repaired, this can lead to a C-to-T transition mutation during replication.
- Incorporation during replication: Although rare, Uracil can be mistakenly incorporated instead of Thymine (T) by DNA polymerases.
The BER pathway efficiently recognizes and removes Uracil from the DNA strand. This process typically involves a DNA glycosylase enzyme that cleaves the glycosidic bond between the Uracil base and the deoxyribose sugar, initiating the repair cascade.
Therefore, Uracil is the specific residue commonly removed by the base excision repair process.