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SNAPc 复合物介导秀丽隐杆线虫饥饿诱导的转剪接。

The SNAPc complex mediates starvation-induced trans-splicing in Caenorhabditis elegans.

机构信息

The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, School of Life Sciences, Ministry of Education Key Laboratory for Membraneless Organelles & Cellular Dynamics, The USTC RNA Institute, Department of Obstetrics and Gynecology, Biomedical Sciences and Health Laboratory of Anhui Province, University of Science and Technology of China, Hefei, Anhui 230001, China.

The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, School of Life Sciences, Ministry of Education Key Laboratory for Membraneless Organelles & Cellular Dynamics, The USTC RNA Institute, Department of Obstetrics and Gynecology, Biomedical Sciences and Health Laboratory of Anhui Province, University of Science and Technology of China, Hefei, Anhui 230001, China.

出版信息

J Genet Genomics. 2022 Oct;49(10):952-964. doi: 10.1016/j.jgg.2022.02.024. Epub 2022 Mar 10.

DOI:10.1016/j.jgg.2022.02.024
PMID:35283340
Abstract

Dietary restriction usually suppresses biosynthesis but activates catabolic pathways in animals. However, the short-term starvation enhances biosynthetic activities and promotes ribosomal biogenesis in adult Caenorhabditis elegans. The mechanism underlying the processes remains largely unknown. Here, we find that the short-term starvation enhances the SL1 trans-splicing of translation-related genes in adult C. elegans by transcriptome analysis. The small nuclear RNA-activating protein complex (SNAPc) promotes SL RNA production and mediates starvation-induced trans-splicing. TOFU-5, a core factor in the upstream sequence transcription complex (USTC) essential for piRNA production, is also involved in the starvation-induced trans-splicing processes. Knocking down components of the SNAPc complex and tofu-5 extends worm survival under starvation conditions. Taken together, our study highlights the importance of SL trans-splicing in the nutrition response and reveals a mechanism of the survival regulation by food deprivation via SNAPc and TOFU-5.

摘要

饮食限制通常会抑制动物的生物合成,但会激活分解代谢途径。然而,短期饥饿会增强生物合成活性,并促进成年秀丽隐杆线虫的核糖体生物发生。这些过程的机制在很大程度上仍然未知。在这里,我们通过转录组分析发现,短期饥饿会增强成年秀丽隐杆线虫中与翻译相关基因的 SL1 反式剪接。小核 RNA 激活蛋白复合物(SNAPc)促进 SL RNA 的产生,并介导饥饿诱导的反式剪接。TOFU-5 是上游序列转录复合物(USTC)的核心因子,对于 piRNA 的产生是必需的,它也参与饥饿诱导的反式剪接过程。敲低 SNAPc 复合物和 tofu-5 的组分可延长饥饿条件下线虫的存活。总之,我们的研究强调了 SL 反式剪接在营养响应中的重要性,并揭示了通过 SNAPc 和 TOFU-5 进行食物剥夺的生存调节机制。

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