Decapping activators Edc3 and Scd6 act redundantly with Dhh1 in post-transcriptional repression of starvation-induced pathways

Rakesh Kumar, Fan Zhang, Shreyas Niphadkar, Chisom Onu, Anil Kumar Vijjamarri, Miriam L Greenberg, Sunil Laxman, Alan G Hinnebusch
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Abstract

Degradation of many yeast mRNAs involves decapping by the Dcp1:Dcp2 complex. Previous studies on decapping activators Edc3 and Scd6 suggested their limited roles in mRNA decay. RNA-seq analysis of mutants lacking one or both proteins revealed that Scd6 and Edc3 have largely redundant activities in targeting numerous mRNAs for degradation that are masked in the single mutants. These transcripts also are frequently targeted by decapping activators Dhh1 and Pat1, and the collective evidence suggests that Scd6/Edc3 act interchangeably to recruit Dhh1 to Dcp2. Ribosome profiling shows that redundancy between Scd6 and Edc3 and their functional interactions with Dhh1 and Pat1 extend to translational repression of particular transcripts, including a cohort of poorly translated mRNAs displaying interdependent regulation by all four factors. Scd6/Edc3 also participate with Dhh1/Pat1 in post-transcriptional repression of proteins required for respiration and catabolism of alternative carbon sources, which are normally expressed only in limiting glucose. Simultaneously eliminating Scd6/Edc3 increases mitochondrial membrane potential and elevates metabolites of the tricarboxylic acid and glyoxylate cycles typically observed only during growth in low glucose. Thus, Scd6/Edc3 act redundantly, in parallel with Dhh1 and in cooperation with Pat1, to adjust gene expression to nutrient availability by controlling mRNA decapping and decay.
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脱帽激活因子Edc3和Scd6与Dhh1在转录后抑制饥饿诱导通路中起冗余作用
许多酵母 mRNA 的降解涉及 Dcp1:Dcp2 复合物的脱帽作用。以前对去凋亡激活因子 Edc3 和 Scd6 的研究表明,它们在 mRNA 降解中的作用有限。对缺乏一种或两种蛋白的突变体进行的 RNA-seq 分析表明,Scd6 和 Edc3 在靶向许多 mRNA 降解方面具有很大程度的冗余活性,而这些活性在单一突变体中被掩盖了。这些转录本也经常被脱帽激活因子 Dhh1 和 Pat1 靶向,综合证据表明,Scd6/Edc3 在将 Dhh1 招募到 Dcp2 上的作用是可以互换的。核糖体分析表明,Scd6 和 Edc3 之间的冗余以及它们与 Dhh1 和 Pat1 的功能性相互作用扩展到了对特定转录本的翻译抑制,包括一组翻译不佳的 mRNA,它们显示了所有四个因子的相互依赖调控。Scd6/Edc3 还与 Dhh1/Pat1 一起参与转录后抑制呼吸作用和替代碳源分解代谢所需的蛋白质,这些蛋白质通常只在葡萄糖限制条件下表达。同时,消除 Scd6/Edc3 会增加线粒体膜电位,并提高三羧酸循环和乙醛酸循环的代谢产物,通常只有在低葡萄糖生长过程中才能观察到。因此,Scd6/Edc3 与 Dhh1 并行并与 Pat1 合作,通过控制 mRNA 的脱帽和衰变,根据营养物质的可用性调整基因表达。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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