RALF1-FERONIA complex affects splicing dynamics to modulate stress responses and growth in plants
RALF1-FERONIA complex affects splicing dynamics to modulate stress responses and growth in plants
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DOI：
10.1126/sciadv.aaz1622
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发表时间：
2020-05-01
期刊：
影响因子：
13.6
通讯作者：
Yu, Feng
中科院分区：
文献类型：
--
作者：
Wang, Long;Yang, Tao;Yu, Feng
通过选择性剪接（AS）将全球转录组变化与植物适应性联系起来的环境响应信号通路仍不清楚。在这里，我们发现细胞外快速碱化因子1（RALF 1）肽与其受体FERONIA（FER）的相互作用，通过与富含甘氨酸的RNA结合蛋白7（GRP 7）相互作用并磷酸化GRP 7，以提高拟南芥中GRP 7的核积累，从而引发快速和大量的RNA AS反应。FER依赖的GRP 7磷酸化增强了其mRNA结合能力及其与剪接体组分U1- 70 K的结合，从而能够选择剪接位点，调节动态AS。RALF 1-FER依赖性剪接靶点的遗传逆转部分挽救了GRP 7缺陷突变体。GRP 7本身的AS诱导了对RALF 1-FER-GRP 7模块的无义介导的衰变反馈，微调了应激反应和细胞生长。RALF 1-FER-GRP 7模块提供了响应于外部刺激的RNA剪接的调节机制的范例。
The environmentally responsive signaling pathways that link global transcriptomic changes through alternative splicing (AS) to plant fitness remain unclear. Here, we found that the interaction of the extracellular rapid alkalinization FACTOR 1 (RALF1) peptide with its receptor FERONIA (FER) triggered a rapid and massive RNA AS response by interacting with and phosphorylating glycine-rich RNA binding protein7 (GRP7) to elevate GRP7 nuclear accumulation in Arabidopsis thaliana. FER-dependent GRP7 phosphorylation enhanced its mRNA binding ability and its association with the spliceosome component U1-70K to enable splice site selection, modulating dynamic AS. Genetic reversal of a RALF1-FER-dependent splicing target partly rescued mutants deficient in GRP7. AS of GRP7 itself induced nonsense-mediated decay feedback to the RALF1-FER-GRP7 module, fine-tuning stress responses, and cell growth. The RALF1-FER-GRP7 module provides a paradigm for regulatory mechanisms of RNA splicing in response to external stimuli.