The role of SLFN11 in DNA replication stress response and its implications for the Fanconi anemia pathway

被引：1

作者：

Mu, Anfeng ^{[1
,2
]}

Okamoto, Yusuke ^{[1
,3
,4
]}

Katsuki, Yoko ^{[1
,5
]}

Takata, Minoru ^{[1
,2
]}

机构：

[1] Kyoto Univ, Radiat Biol Ctr, Grad Sch Biostudies, Lab DNA Damage Signaling,Dept Late Effects Studies, Kyoto, Japan

[2] Kyoto Univ, Multilayer Network Res Unit, Res Coordinat Alliance, Kyoto, Japan

[3] Kyoto Univ, Grad Sch Med, Dept Hematol & Oncol, Kyoto, Japan

[4] Mt Sinai Hosp, Lunenfeld Tanenbaum Res Inst, Toronto, ON, Canada

[5] Kyushu Univ, Grad Sch Pharmaceut Sci, Dept Cellular Biochem, Fukuoka, Japan

来源：

DNA REPAIR | 2024年 / 141卷

关键词：

Fanconi anemia; SLFN11; Replication stress; RAD51; Hematopoiesis; DAMAGE; SCHLAFEN; FORMALDEHYDE; ACTIVATION; CHECKPOINT; ALDEHYDES; HELICASE; FAMILY; REPAIR;

D O I：

10.1016/j.dnarep.2024.103733

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

Fanconi anemia (FA) is a hereditary disorder characterized by a deficiency in the repair of DNA interstrand crosslinks and the response to replication stress. Endogenous DNA damage, most likely caused by aldehydes, severely affects hematopoietic stem cells in FA, resulting in progressive bone marrow failure and the development of leukemia. Recent studies revealed that expression levels of SLFN11 affect the replication stress response and are a strong determinant in cell killing by DNA-damaging cancer chemotherapy. Because SLFN11 is highly expressed in the hematopoietic system, we speculated that SLFN11 may have a significant role in FA pathophysiology. Indeed, we found that DNA damage sensitivity in FA cells is significantly mitigated by the loss of SLFN11 expression. Mechanistically, we demonstrated that SLFN11 destabilizes the nascent DNA strands upon replication fork stalling. In this review, we summarize our work regarding an interplay between SLFN11 and the FA pathway, and the role of SLFN11 in the response to replication stress.

引用

页数：11

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