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mRNA 输出接头蛋白 Yra1 通过其 C 盒结构域促进 DNA 双链断裂修复。

The mRNA export adaptor Yra1 contributes to DNA double-strand break repair through its C-box domain.

机构信息

Dept. of Cell Biology, 30 Quai E. Ansermet, University of Geneva, Geneva, Switzerland.

Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, NY, United States of America.

出版信息

PLoS One. 2019 Apr 5;14(4):e0206336. doi: 10.1371/journal.pone.0206336. eCollection 2019.

DOI:10.1371/journal.pone.0206336
PMID:30951522
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6450643/
Abstract

Yra1 is an mRNA export adaptor involved in mRNA biogenesis and export in S. cerevisiae. Yra1 overexpression was recently shown to promote accumulation of DNA:RNA hybrids favoring DNA double strand breaks (DSB), cell senescence and telomere shortening, via an unknown mechanism. Yra1 was also identified at an HO-induced DSB and Yra1 depletion causes defects in DSB repair. Previous work from our laboratory showed that Yra1 ubiquitination by Tom1 is important for mRNA export. Here, we found that Yra1 is also ubiquitinated by the SUMO-targeted ubiquitin ligases Slx5-Slx8 implicated in the interaction of irreparable DSB with nuclear pores. We further show that Yra1 binds an HO-induced irreparable DSB in a process dependent on resection. Importantly, a Yra1 mutant lacking the evolutionarily conserved C-box is not recruited to an HO-induced irreparable DSB and becomes lethal under DSB induction in a HO-cut reparable system. Together, the data provide evidence that Yra1 plays a crucial role in DSB repair via homologous recombination. While Yra1 sumoylation and/or ubiquitination are dispensable, the Yra1 C-box region is essential in this process.

摘要

Yra1 是一种 mRNA 输出衔接子，参与 mRNA 的生物发生和输出过程。最近的研究表明，Yra1 过表达通过未知机制促进 DNA:RNA 杂交体的积累，从而导致 DNA 双链断裂 (DSB)、细胞衰老和端粒缩短。Yra1 还在 HO 诱导的 DSB 处被鉴定出来，并且 Yra1 的耗竭会导致 DSB 修复缺陷。我们实验室之前的工作表明，Tom1 对 Yra1 的泛素化对于 mRNA 输出很重要。在这里，我们发现 Yra1 还被 SUMO 靶向泛素连接酶 Slx5-Slx8 修饰，该酶参与不可修复的 DSB 与核孔的相互作用。我们进一步表明，Yra1 在依赖于切除的过程中结合 HO 诱导的不可修复 DSB。重要的是，缺乏进化上保守的 C 盒的 Yra1 突变体不能被招募到 HO 诱导的不可修复 DSB 处，并且在 HO 切割可修复系统中诱导 DSB 时会变得致命。总之，这些数据提供了证据表明，Yra1 通过同源重组在 DSB 修复中发挥关键作用。虽然 Yra1 的 SUMO 化和/或泛素化是可有可无的，但 Yra1 的 C 盒区域在这个过程中是必不可少的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ddc/6450643/564549f4f872/pone.0206336.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ddc/6450643/4a92a34365b5/pone.0206336.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ddc/6450643/0beda7fa1828/pone.0206336.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ddc/6450643/6e07a4ab25d7/pone.0206336.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ddc/6450643/564549f4f872/pone.0206336.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ddc/6450643/4a92a34365b5/pone.0206336.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ddc/6450643/0beda7fa1828/pone.0206336.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ddc/6450643/6e07a4ab25d7/pone.0206336.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ddc/6450643/564549f4f872/pone.0206336.g004.jpg

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