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复制性DNA聚合酶ε和δ全酶在人类基因组的G-四链体处表现出广泛的抑制作用。

Replicative DNA polymerase epsilon and delta holoenzymes show wide-ranging inhibition at G-quadruplexes in the human genome.

作者信息

Hile Suzanne E, Weissensteiner Matthias H, Pytko Kara G, Dahl Joseph, Kejnovsky Eduard, Kejnovská Iva, Hedglin Mark, Georgakopoulos-Soares Ilias, Makova Kateryna D, Eckert Kristin A

机构信息

Department of Pathology, The Jake Gittlen Laboratories for Cancer Research, Penn State University College of Medicine, Hershey, PA 17033, United States.

Department of Biology, Penn State University Eberly College of Science, University Park, PA 16802, United States.

出版信息

Nucleic Acids Res. 2025 Apr 22;53(8). doi: 10.1093/nar/gkaf352.

Abstract

G-quadruplexes (G4s) are functional elements of the human genome, some of which inhibit DNA replication. We investigated replication of G4s within highly abundant microsatellite (GGGA, GGGT) and transposable element (L1 and SVA) sequences. We found that genome-wide, numerous motifs are located preferentially on the replication leading strand and the transcribed strand templates. We directly tested replicative polymerase ϵ and δ holoenzyme inhibition at these G4s, compared to low abundant motifs. For all G4s, DNA synthesis inhibition was higher on the G-rich than C-rich strand or control sequence. No single G4 was an absolute block for either holoenzyme; however, the inhibitory potential varied over an order of magnitude. Biophysical analyses showed the motifs form varying topologies, but replicative polymerase inhibition did not correlate with a specific G4 structure. Addition of the G4 stabilizer pyridostatin severely inhibited forward polymerase synthesis specifically on the G-rich strand, enhancing G/C strand asynchrony. Our results reveal that replicative polymerase inhibition at every G4 examined is distinct, causing complementary strand synthesis to become asynchronous, which could contribute to slowed fork elongation. Altogether, we provide critical information regarding how replicative eukaryotic holoenzymes navigate synthesis through G4s naturally occurring thousands of times in functional regions of the human genome.

摘要

G-四链体(G4s)是人类基因组的功能元件,其中一些会抑制DNA复制。我们研究了高度丰富的微卫星序列(GGGA、GGGT)和转座元件序列(L1和SVA)中的G4s的复制情况。我们发现,在全基因组范围内,许多基序优先位于复制前导链和转录链模板上。与低丰度基序相比,我们直接测试了这些G4s对复制性聚合酶ε和δ全酶的抑制作用。对于所有G4s,富含鸟嘌呤的链上的DNA合成抑制作用高于富含胞嘧啶的链或对照序列。没有单个G4对任何一种全酶构成绝对障碍;然而,抑制潜力在一个数量级内变化。生物物理分析表明,这些基序形成了不同的拓扑结构,但复制性聚合酶抑制作用与特定的G-四链体结构无关。添加G4稳定剂吡啶司他汀会严重抑制正向聚合酶在富含鸟嘌呤链上的合成,增强G/C链的异步性。我们的结果表明,在所检测的每个G4处,复制性聚合酶的抑制作用都是不同的,导致互补链合成变得异步,这可能会导致叉延伸减慢。总之,我们提供了关于真核生物复制全酶如何在人类基因组功能区域中自然存在数千次的G4s上进行合成导航的关键信息。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4db5/12038398/d588cfa0a745/gkaf352figgra1.jpg

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