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XP is an autosomal recessive disorder with 100% penetrance and can result from mutations in any one of eight genes.The products of seven of these genes (XP-A through G) are involved in the repair of ultraviolet-induced photoproducts in DNA by the process of nucleotide excision repair (NER) [5].XPA protein verifies that proteins are in the correct position and then the nucleases XPG and XPF cut the DNA on either side of the damage, so that the damaged section can be removed and replaced with intact DNA.The XPC and XPE proteins are needed to recognise the photoproducts in DNA.XPB and XPD are part of a protein complex TFIIH, which opens up the structure of the DNA around the site of the photoproduct.
XP is an autosomal recessive disorder with 100% penetrance and can result from mutations in any one of eight genes. The products of seven of these genes (XP-A through G) are involved in the repair of ultraviolet-induced photoproducts in DNA by the process of nucleotide excision repair (NER) [5]. The XPC and XPE proteins are needed to recognise the photoproducts in DNA. XPB and XPD are part of a protein complex TFIIH, which opens up the structure of the DNA around the site of the photoproduct. XPA protein verifies that proteins are in the correct position and then the nucleases XPG and XPF cut the DNA on either side of the damage, so that the damaged section can be removed and replaced with intact DNA.
There are two branches of NER, designated transcription-coupled repair, which rapidly repairs areas of DNA that are "active" and being transcribed into RNA, and global genome repair, which repairs damage in the rest of the genome more slowly. XPC and XPE proteins are only required for the latter branch, whereas all the other XP proteins are required for both branches. Probably as a consequence of this, patients defective in the XPC or XPE genes do not, in general, have the extreme sunburn reactions or neurological abnormalities described above.
Defects in the eighth XP gene do not affect NER. Instead these so-called XP variants (XP-V) have problems replicating DNA containing ultraviolet-induced damage [9]. DNA replication is carried out by DNA polymerases. The DNA polymerases that normally replicate DNA cannot deal with damage in the DNA template and specialised polymerases have to be employed to get past the damage (translesion synthesis). For UV damage, the cell uses DNA polymerase η, encoded by the gene POLH and it is this gene that is mutated in XP-V patients [10]. Like XP-C and XP-E patients, XP-V patients rarely have extreme sunburn reactions or neurological problems.
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