Chromatin-remodeling factor BAZ1A/ACF1 targets UV damage sites in an MLL1-dependent manner to facilitate nucleotide excision repair

被引:8
作者
Koyauchi, Takafumi [1 ,2 ]
Niida, Hiroyuki [1 ]
Motegi, Akira [3 ]
Sakai, Satoshi [1 ]
Uchida, Chiharu [4 ]
Ohhata, Tatsuya [1 ]
Iijima, Kenta [5 ]
Yokoyama, Akihiko [6 ]
Suda, Takafumi [2 ]
Kitagawa, Masatoshi [1 ]
机构
[1] Hamamatsu Univ Sch Med, Dept Mol Biol, 1-20-1 Handayama,Higashi Ku, Hamamatsu, Shizuoka 4313192, Japan
[2] Hamamatsu Univ, Dept Internal Med, Div 2, Sch Med, 1-20-1 Handayama,Higashi Ku, Hamamatsu, Shizuoka 4313192, Japan
[3] Kyoto Univ, Dept Radiat Genet, Grad Sch Med, Yoshida Konoe cho,Sakyo Ku, Kyoto 6068501, Japan
[4] Hamamatsu Univ, Preeminent Med Photon Educ & Res Ctr, Adv Res Facil & Serv, Sch Med, 1-20-1 Handayama,Higashi Ku, Hamamatsu, Shizuoka 4313192, Japan
[5] Hamamatsu Univ Sch Med, Preeminent Med Photon Educ & Res Ctr, Lab Anim Facil & Serv, 1-20-1 Handayama,Higashi ku, Hamamatsu, Shizuoka 4313192, Japan
[6] Natl Canc Ctr, Tsuruoka Metabol Lab, Tsuruoka, Yamagata 9970052, Japan
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH | 2022年 / 1869卷 / 11期
关键词
MLL1; BAZ1A; HBO1; Ultraviolet; DNA-BINDING-PROTEIN; H3; ACETYLATION; PHD FINGER; XPC; RECOGNITION; COMPLEX; TUMOR; TFIIH; MLL; PHOSPHORYLATION;
D O I
10.1016/j.bbamcr.2022.119332
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Ultraviolet (UV) light irradiation generates pyrimidine dimers on DNA, such as cyclobutane pyrimidine dimers (CPDs) and (6-4) photoproducts. Such dimers distort the high-order DNA structure and prevent transcription and replication. The nucleotide excision repair (NER) system contributes to resolving this type of DNA lesion. There are two pathways that recognize pyrimidine dimers. One acts on transcribed strands of DNA (transcription -coupled NER), and the other acts on the whole genome (global genome-NER; GG-NER). In the latter case, DNA damage-binding protein 2 (DDB2) senses pyrimidine dimers with several histone modification enzymes. We previously reported that histone acetyltransferase binding to ORC1 (HBO1) interacts with DDB2 and facilitates recruitment of the imitation switch chromatin remodeler at UV-irradiated sites via an unknown methyl-transferase. Here, we found that the phosphorylated histone methyltransferase mixed lineage leukemia 1 (MLL1) was maintained at UV-irradiated sites in an HBO1-dependent manner. Furthermore, MLL1 catalyzed histone H3K4 methylation and recruited the chromatin remodeler bromodomain adjacent to zinc finger domain 1A (BAZ1A)/ATP-utilizing chromatin assembly and remodeling factor 1 (ACF1). Depletion of MLL1 suppressed BAZ1A accumulation at UV-irradiated sites and inhibited the removal of CPDs. These data indicate that the DDB2-HBO1-MLL1 axis is essential for the recruitment of BAZ1A to facilitate GG-NER.
引用
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页数:13
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