DICER- and MMSET-catalyzed H4K20me2 recruits the nucleotide excision repair factor XPA to DNA damage sites
Autor: | Holger Richly, Shalaka Chitale |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Ribonuclease III DNA Repair DNA damage DNA repair Ultraviolet Rays genetic processes Article DEAD-box RNA Helicases Histones 03 medical and health sciences Cell Line Tumor Humans Research Articles biology Lysine fungi Endoribonuclease Dicer food and beverages Cell Biology DNA Repair Pathway Histone-Lysine N-Methyltransferase Cell biology Chromatin Xeroderma Pigmentosum Group A Protein Repressor Proteins enzymes and coenzymes (carbohydrates) 030104 developmental biology Histone HEK293 Cells biology.protein Biocatalysis Dicer Nucleotide excision repair DNA Damage |
Zdroj: | The Journal of Cell Biology |
ISSN: | 1540-8140 0021-9525 |
Popis: | The endoribonuclease DICER facilitates chromatin decondensation during lesion recognition following UV exposure. Chitale and Richly show that DICER mediates the recruitment of the methyltransferase MMSET, which catalyzes the dimethylation of histone H4 at lysine 20 and facilitates the recruitment of the nucleotide excision repair factor XPA. Ultraviolet (UV) irradiation triggers the recruitment of DNA repair factors to the lesion sites and the deposition of histone marks as part of the DNA damage response. The major DNA repair pathway removing DNA lesions caused by exposure to UV light is nucleotide excision repair (NER). We have previously demonstrated that the endoribonuclease DICER facilitates chromatin decondensation during lesion recognition in the global-genomic branch of NER. Here, we report that DICER mediates the recruitment of the methyltransferase MMSET to the DNA damage site. We show that MMSET is required for efficient NER and that it catalyzes the dimethylation of histone H4 at lysine 20 (H4K20me2). H4K20me2 at DNA damage sites facilitates the recruitment of the NER factor XPA. Our work thus provides evidence for an H4K20me2-dependent mechanism of XPA recruitment during lesion recognition in the global-genomic branch of NER. |
Databáze: | OpenAIRE |
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