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解旋酶/ SUMO 靶向泛素连接酶 Uls1 与 Holliday 连接点解旋酶 Yen1 相互作用。

Helicase/SUMO-targeted ubiquitin ligase Uls1 interacts with the Holliday junction resolvase Yen1.

机构信息

Department of Molecular Biosciences, the Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.

出版信息

PLoS One. 2019 Mar 21;14(3):e0214102. doi: 10.1371/journal.pone.0214102. eCollection 2019.

Abstract

Resolution of branched DNA structures is pivotal for repair of stalled replication forks and meiotic recombination intermediates. The Yen1 nuclease cleaves both Holliday junctions and replication forks. We show that Yen1 interacts physically with Uls1, a suggested SUMO-targeted ubiquitin ligase that also contains a SWI/SNF-family ATPase-domain. Yen1 is SUMO-modified in its noncatalytic carboxyl terminus and DNA damage induces SUMOylation. SUMO-modification of Yen1 strengthens the interaction to Uls1, and mutations in SUMO interaction motifs in Uls1 weakens the interaction. However, Uls1 does not regulate the steady-state level of SUMO-modified Yen1 or chromatin-associated Yen1. In addition, SUMO-modification of Yen1 does not affect the catalytic activity in vitro. Consistent with a shared function for Uls1 and Yen1, mutations in both genes display similar phenotypes. Both uls1 and yen1 display negative genetic interactions with the alternative HJ-cleaving nuclease Mus81, manifested both in hypersensitivity to DNA damaging agents and in meiotic defects. Point mutations in ULS1 (uls1K975R and uls1C1330S, C1333S) predicted to inactivate the ATPase and ubiquitin ligase activities, respectively, are as defective as the null allele, indicating that both functions of Uls1 are essential. A micrococcal nuclease sequencing experiment showed that Uls1 had minimal effects on global nucleosome positioning/occupancy. Moreover, increased gene dosage of YEN1 partially alleviates the mus81 uls1 sensitivity to DNA damage. We suggest a preliminary model in which Uls1 acts in the same pathway as Yen1 to resolve branched DNA structures.

摘要

分叉 DNA 结构的解决对于修复停滞的复制叉和减数分裂重组中间体至关重要。 Yen1 核酸内切酶可切割霍利迪连接点和复制叉。我们表明 Yen1 与 Uls1 物理相互作用,Uls1 是一种推定的 SUMO 靶向泛素连接酶,也含有 SWI/SNF 家族 ATPase 结构域。 Yen1 在其非催化羧基末端被 SUMO 修饰,并且 DNA 损伤诱导 SUMOylation。 Yen1 的 SUMO 修饰增强了与 Uls1 的相互作用,并且 Uls1 中的 SUMO 相互作用基序突变削弱了相互作用。然而,Uls1 不调节 Yen1 的 SUMO 修饰的稳态水平或染色质相关的 Yen1。此外, Yen1 的 SUMO 修饰不影响体外的催化活性。与 Uls1 和 Yen1 具有共同功能一致,这两个基因的突变都显示出相似的表型。 uls1 和 yen1 都与替代 HJ 切割核酸内切酶 Mus81 发生负遗传相互作用,表现在对 DNA 损伤剂的敏感性增加和减数分裂缺陷。分别预测使 ATPase 和泛素连接酶活性失活的 ULS1 点突变(uls1K975R 和 uls1C1330S、C1333S)与 null 等位基因一样有缺陷,表明 Uls1 的两个功能都是必不可少的。微球菌核酸酶测序实验表明 Uls1 对全局核小体定位/占据几乎没有影响。此外, YEN1 的基因剂量增加部分缓解了 mus81 uls1 对 DNA 损伤的敏感性。我们提出了一个初步模型,其中 Uls1 与 Yen1 一起作用于解决分叉 DNA 结构的同一途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c3f/6428284/1de04eff15a2/pone.0214102.g001.jpg

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