Autophagy contributes to positive feedback regulation of SnRK1 signaling in plants.

IF 14.6 1区 生物学 Q1 CELL BIOLOGY Autophagy Pub Date : 2023-12-01 Epub Date: 2023-08-20 DOI:10.1080/15548627.2023.2247741
Chao Yang, Xibao Li, Jun Zhou, Caiji Gao
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Abstract

SnRK1 (SNF1-related protein kinase 1) is a plant ortholog of yeast Snf1 and mammalian adenosine monophosphate-activated protein kinase (AMPK) that acts as a positive regulator of macroautophagy/autophagy. However, whether and how the autophagy pathway modulates SnRK1 activity remains elusive. Recently, we identified a clade of plant-specific FLZ (FCS-like zinc finger) proteins as novel ATG8 (autophagy-related 8)-interacting partners in Arabidopsis thaliana. These AtFLZs, which mainly localize on the surface of mitochondria, can inhibit SnRK1 signaling by repressing the T-loop phosphorylation of its catalytic α subunits, thereby negatively regulating carbon starvation-induced autophagy and plant tolerance to energy deprivation. Upon energy starvation, autophagy is activated to mediate the degradation of these AtFLZs, thus relieving their repression of SnRK1. More importantly, the ATG8-FLZ-SnRK1 regulatory axis appears to be functionally conserved during seed plant evolution. These findings highlight the positive role of autophagy in SnRK1 signaling activation under energy-limiting conditions in plants.Abbreviations: ADS, AIMs docking site; AIM, ATG8-interacting motif; AMPK, adenosine monophosphate-activated protein kinase; ATG, autophagy-related; ESCRT, endosomal sorting complexes required for transport; FLZ, FCS-like zinc finger protein; FREE1, FYVE DOMAIN PROTEIN REQUIRED FOR ENDOSOMAL SORTING 1; RAPTOR, REGULATORY-ASSOCIATED PROTEIN OF TOR; Snf1, SUCROSE NON-FERMENTING 1; SnRK1, SNF1-related kinase 1; TOR, TARGET OF RAPAMYCIN.

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自噬有助于植物中SnRK1信号的正反馈调节。
SnRK1(SNF1相关蛋白激酶1)是酵母SNF1和哺乳动物腺苷酸活化蛋白激酶(AMPK)的植物直系同源物,作为大细胞自噬/自噬的阳性调节因子。然而,自噬途径是否以及如何调节SnRK1活性仍然难以捉摸。最近,我们在拟南芥中鉴定了一个植物特异性FLZ(FCS样锌指)蛋白分支作为新的ATG8(自噬相关8)相互作用伙伴。这些主要定位于线粒体表面的AtFLZ可以通过抑制其催化α亚基的T环磷酸化来抑制SnRK1信号传导,从而负调控碳饥饿诱导的自噬和植物对能量剥夺的耐受性。在能量饥饿时,自噬被激活以介导这些AtFLZ的降解,从而减轻它们对SnRK1的抑制。更重要的是,ATG8-FLZ-SnRK1调控轴在种子植物进化过程中似乎是功能保守的。这些发现强调了自噬在植物能量限制条件下SnRK1信号激活中的积极作用。缩写:ADS、AIMs对接点;AIM,ATG8相互作用基序;AMPK,一磷酸腺苷活化蛋白激酶;ATG,自噬相关;ESCRT,运输所需的内体分选复合物;FLZ、FCS样锌指蛋白;内体分选1所需的游离1、FYVE结构域蛋白;猛禽,猛禽的调节相关蛋白;Snf1,蔗糖非发酵1;SnRK1、SNF1相关激酶1;TOR,雷帕霉素的靶标。
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来源期刊
Autophagy
Autophagy 生物-细胞生物学
CiteScore
21.30
自引率
2.30%
发文量
277
审稿时长
1 months
期刊介绍: Autophagy is a peer-reviewed journal that publishes research on autophagic processes, including the lysosome/vacuole dependent degradation of intracellular material. It aims to be the premier journal in the field and covers various connections between autophagy and human health and disease, such as cancer, neurodegeneration, aging, diabetes, myopathies, and heart disease. Autophagy is interested in all experimental systems, from yeast to human. Suggestions for specialized topics are welcome. The journal accepts the following types of articles: Original research, Reviews, Technical papers, Brief Reports, Addenda, Letters to the Editor, Commentaries and Views, and Articles on science and art. Autophagy is abstracted/indexed in Adis International Ltd (Reactions Weekly), EBSCOhost (Biological Abstracts), Elsevier BV (EMBASE and Scopus), PubMed, Biological Abstracts, Science Citation Index Expanded, Web of Science, and MEDLINE.
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