Abstract
ABSTRACTThe integrity of the genome is maintained by specific DNA repair pathways. The main pathway removing DNA lesions induced by exposure to UV light is nucleotide excision repair (NER). The DNA damage response at chromatin is accompanied by the recruitment of DNA repair factors to the lesion site and the deposition of specific histone marks. The function of these histone marks in NER stays for the most part elusive. We have recently reported that the methyltransferase MMSET catalyzes the dimethylation of histone H4 at lysine 20 (H4K20me2) at the lesion site. The deposition of H4K20me2 at DNA damage sites elicits the recruitment of the NER factor XPA providing evidence for an H4K20me2-dependent DNA repair factor recruitment mechanism during lesion recognition in the global-genomic branch of NER. Here we discuss how H4K20me2 might impact on the chromatin conformation and the DNA damage response.
Highlights
The integrity of the genome is maintained by specific DNA repair pathways
The Repair-Prime-Access model [1] suggests that DNA repair consists of three major steps, decondensation of chromatin, access of the repair machinery and repair
We have recently reported that a specific chromatin mark, H4K20me2, promotes the recruitment of XPA to the DNA damage site (Figure 1)
Summary
The integrity of the genome is maintained by specific DNA repair pathways. The main pathway removing DNA lesions induced by exposure to UV light is nucleotide excision repair (NER). Nucleotide excision repair may result in chromatin decondensation of several kilobases of DNA around the lesions site [2]. XPA forms a critical link between the recognition of the lesion, modifications in chromatin structure [9], and recruitment of XPB, XPF, XPG and the entire core repair machinery that can excise and resynthesize the damaged stretch of DNA. XPA interacts with both the damage recognition machinery i.e. proteins like DDB2 and XPC, as well as the downstream repair machinery i.e factors like RPA and XPF.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
