Fibrillarin promotes homologous recombination repair by facilitating the recruitment of recombinase RAD51 to DNA damage sites.

Yanhua MU; Jinhua Han; Mingjie WU; Zongfang LI; Ke DU; Yameng Wei; Mengjie WU; Jun Huang

Return

Fibrillarin promotes homologous recombination repair by facilitating the recruitment of recombinase RAD51 to DNA damage sites.

Author: Yanhua MU ¹ ; Jinhua HAN ² ; Mingjie WU ³ ; Zongfang LI ¹ ; Ke DU ¹ ; Yameng WEI ¹ ; Mengjie WU ⁴ ; Jun HUANG ⁵
Author Information

1. National-Local Joint Engineering Research Center of Biodiagnosis & Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, China.
2. Zhejiang Provincial Key Lab of Geriatrics and Geriatrics Institute of Zhejiang Province, Department of Geriatrics, Zhejiang Hospital, Hangzhou 310030, China.
3. Trauma Center, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China.
4. The Affiliated Hospital of Stomatology, School of Stomatology, Zhejiang University School of Medicine, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Hangzhou 310006, China. jhuang@zju.edu.cn, wumengjie@zju.edu.cn.
5. Zhejiang Provincial Key Lab of Geriatrics and Geriatrics Institute of Zhejiang Province, Department of Geriatrics, Zhejiang Hospital, Hangzhou 310030, China. jhuang@zju.edu.cn.
Publication Type:Journal Article
MeSH: Recombinational DNA Repair; DNA-Binding Proteins/metabolism*; DNA Repair; DNA Damage; DNA
From: Journal of Zhejiang University. Science. B 2023;24(12):1165-1173
CountryChina
Language:English
Abstract: Eukaryotic organisms constantly face a wide range of internal and external factors that cause damage to their DNA. Failure to accurately and efficiently repair these DNA lesions can result in genomic instability and the development of tumors (Canela et al., 2017). Among the various forms of DNA damage, DNA double-strand breaks (DSBs) are particularly harmful. Two major pathways, non-homologous end joining (NHEJ) and homologous recombination (HR), are primarily responsible for repairing DSBs (Katsuki et al., 2020; Li and Yuan, 2021; Zhang and Gong, 2021; Xiang et al., 2023). NHEJ is an error-prone repair mechanism that simply joins the broken ends together (Blunt et al., 1995; Hartley et al., 1995). In contrast, HR is a precise repair process. It involves multiple proteins in eukaryotic cells, with the RAD51 recombinase being the key player, which is analogous to bacterial recombinase A (RecA) (Shinohara et al., 1992). The central event in HR is the formation of RAD51-single-stranded DNA (ssDNA) nucleoprotein filaments that facilitate homology search and DNA strand invasion, ultimately leading to the initiation of repair synthesis (Miné et al., 2007; Hilario et al., 2009; Ma et al., 2017).