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LncRNA-dependent nuclear stress bodies promote intron retention through SR protein phosphorylation
Title: | LncRNA-dependent nuclear stress bodies promote intron retention through SR protein phosphorylation |
Authors: | Ninomiya, Kensuke Browse this author →KAKEN DB | Adachi, Shungo Browse this author | Natsume, Tohru Browse this author →KAKEN DB | Iwakiri, Junichi Browse this author →KAKEN DB | Terai, Goro Browse this author | Asai, Kiyoshi Browse this author →KAKEN DB | Hirose, Tetsuro Browse this author →KAKEN DB |
Keywords: | intron retention | noncoding RNA | nuclear stress bodies | phosphorylation | splicing factors |
Issue Date: | 3-Feb-2020 |
Publisher: | John Wiley & Sons |
Journal Title: | EMBO Journal |
Volume: | 39 |
Issue: | 23 |
Start Page: | e102729 |
Publisher DOI: | 10.15252/embj.2019102729 |
Abstract: | A number of long noncoding RNAs (lncRNAs) are induced in response to specific stresses to construct membrane-less nuclear bodies; however, their function remains poorly understood. Here, we report the role of nuclear stress bodies (nSBs) formed on highly repetitive satellite III (HSATIII) lncRNAs derived from primate-specific satellite III repeats upon thermal stress exposure. A transcriptomic analysis revealed that depletion of HSATIII lncRNAs, resulting in elimination of nSBs, promoted splicing of 533 retained introns during thermal stress recovery. A HSATIII-Comprehensive identification of RNA-binding proteins by mass spectrometry (ChIRP-MS) analysis identified multiple splicing factors in nSBs, including serine and arginine-rich pre-mRNA splicing factors (SRSFs), the phosphorylation states of which affect splicing patterns. SRSFs are rapidly de-phosphorylated upon thermal stress exposure. During stress recovery, CDC like kinase 1 (CLK1) was recruited to nSBs and accelerated the re-phosphorylation of SRSF9, thereby promoting target intron retention. Our findings suggest that HSATIII-dependent nSBs serve as a conditional platform for phosphorylation of SRSFs by CLK1 to promote the rapid adaptation of gene expression through intron retention following thermal stress exposure. |
Rights: | This is the peer reviewed version of the following article: The EMBO Journal: 39(3): e102729., which has been published in final form at https://doi.org/10.15252/embj.2019102729. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions. |
Type: | article (author version) |
URI: | http://hdl.handle.net/2115/79022 |
Appears in Collections: | 遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 廣瀬 哲郎
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