Perception of Pyrimidine Dimers Removal Mechanisms
Pyrimidine dimers are DNA lesions resulting from the direct effect of ultraviolet (UV) radiation, and describe covalent bonds between adjacent thymines or cytosines in dna. These dimers interfere with normal DNA replication and transcription, thereby adding significant risks to cellular integrity and functionality. One of the main methods used to excise such lesions from the DNA is nucleotide excision repair (NER), a highly complex multi-enzyme process involving several proteins, which finally leads to complete restoration of an intact DNA molecule .pyrimidine dimer (ad)
Pathways of nucleotide excision repair
The NER acts at recognizing the dimerized nucleotides and cuts out the damaged DNA HELP SEGMENT. The original process starts by arranging a collection of numerous proteins, such as XPA, XPC and an assembly known as the TFIIH complex which melts the DNA containing that injury. Afterwards, some specific endonucleases like XPF/XPG play a role in cleaving these lesions on both sides. It contains about 30 nucleotides excised from the DNA as a complex with repair factors. This means that the break in the DNA strand can be repaired by DNA polymerases, using the intact complementary strand as a template .
Repair mechanisms in Comparison to other OrganismsComments.
Unlike any other species, which utilize NER alone to repair pyrimidine dimers, humans have unique strategies. For example, some bacteria use the enzyme photolyase which does exactly repair by mediating their photoreactivation (direct reversal of pyrimidine dimer formation). This mechanism is unique to three quality meiosis in comparison to NER and oophorectomy, which presents evolutionary adaptations for prevention of UV exposure as a result156. Similarly, analysis of excision repair pathways using yeast models provided insight into genes that are essential for an efficient damage response34.
What Happens When a Repair Fails
The failure in repairing the pyrimidine dimers leads mutations and cancer. Integration of these pathways is not only informative regarding the cellular response to UV damage, but also has implications for possible therapeutic strategies towards boosting DNA repair pathways in human245.
Nucleotide excision repair is the major pathway that repairs pyrimidine dimers in humans; however, the many forms of DNA repair seen throughout biology are a testament to the complexity of damage response systems.
