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在同类重组缺陷细胞的基切除修复过程中,HMCES破坏了复制叉的稳定性
María José Peña-Gómez1,2, Yaiza Rodríguez-Martín1,2, Marta Del Rio Oliva1,2
1Centro Andaluz de Biología Molecular y Medicina Regenerativa (CABIMER) Universidad de Sevilla-CSIC-Universidad Pablo de Olavide, Seville 41092, Spain.
Science advances
|March 26, 2025
概括
同类重组缺陷 (HRD) 细胞因DNA损伤而面临复制的不稳定性. 蛋白质HMCES通过形成DNA-蛋白质交叉链接来加剧这种情况,导致HRD瘤的基因组不稳定性.
科学领域:
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
- 修复DNA修复DNA的修复
背景情况:
- 阿普里尼克/阿普里米尼克 (AP) 位点和单链断裂可能会损害复制的稳定性,特别是在同源重组缺陷 (HRD) 细胞中.
- 众所周知,蛋白质HMCES可以调节DNA模板链上的模板AP位的复制分叉速度.
研究的目的:
- 研究HMCES在复制过程中的新生DNA链上的作用.
- 确定HMCES-DNA-蛋白质交叉链接 (DPCs) 对受损核基的基切除修复 (BER) 的影响.
主要方法:
- 研究了HMCES对HRD细胞复制分叉动态的影响.
- 在BER期间评估了从5-hydroxymethyl-2'-deoxycytidine (5hmdC) 中衍生的5-hydroxymethyl-2'-deoxyuridine的去除.
- 利用HMCES枯竭来评估其对细胞缺陷的影响.
主要成果:
- HMCES-DPCs阻碍了从复制分叉中获得的5hmdC衍生病变的BER介导的去除.
- HRD细胞表现出高水平的HMCES-DPCs,在5hmdC暴露时增加.
- 在HRD细胞中,HMCES枯竭显著减少了5hmdC诱导的复制叉缺陷,染色体异常和细胞死亡.
结论:
- HMCES-DPCs是单链DNA缺口的重要来源,由BER启动.
- 内生HMCES-DPCs有助于HRD瘤中的基因组不稳定性.
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