Abstract

Target of rapamycin (TOR) acts as a master regulator in coordination of cell growth with energy and nutrient availability. Despite the increased appreciation of the essential role of the TOR complex in interaction with phytohormone signaling, little is known about its function on ethylene signaling. Here, through expression analysis, genetic and biochemical approaches, we reveal that TOR functions in the regulation of ethylene signals. Transcriptional analysis indicates that TOR inhibition by AZD8055 upregulated senescence- and ethylene-related genes expression. Furthermore, ethylene insensitive mutants like etr1-1, ein2-5 and ein3 eil1, showed more hyposensitivity to AZD8055 than that of WT in hypocotyl growth inhibition. Similarly, blocking ethylene signals by ethylene action inhibitor Ag+ or biosynthesis inhibitor aminoethoxyvinylglycine (AVG) largely rescued hypocotyl growth even in presence of AZD8055. In addition, we also demonstrated that Type 2A phosphatase-associated protein of 46 kDa (TAP46), a downstream component of TOR signaling, physically interacts with 1-aminocy-clopropane-1-carboxylate (ACC) synthase ACS2 and ACS6. Arabidopsis overexpressing ACS2 or ACS6 showed more hypersensitivity to AZD8055 than WT in hypocotyl growth inhibition. Moreover, ACS2/ACS6 protein was accumulated under TOR suppression, implying TOR modulates ACC synthase protein levels. Taken together, our results indicate that TOR participates in negatively modulating ethylene signals and the molecular mechanism is likely involved in the regulation of ethylene biosynthesis by affecting ACSs in transcription and protein levels.

Highlights

  • Target of rapamycin (TOR), an evolutionarily conserved serine/threonine protein kinase, plays an essential role in controlling cell growth and maintaining cellular homeostasis in response to nutrition and energy availability in eukaryotes [1,2,3]

  • It has been reported that rapamycin can significantly delay senescence in FK506-binding protein 12 kD (FKBP12)-expressing plants [28], many studies showed that severe suppression of TOR accelerated leaves chlorosis or senescence in the growing plants [13,33,59]

  • We found that many ethylene associated genes involved in biosynthesis and response displayed consistent up-regulation under TOR inhibition

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Summary

Introduction

Target of rapamycin (TOR), an evolutionarily conserved serine/threonine protein kinase, plays an essential role in controlling cell growth and maintaining cellular homeostasis in response to nutrition and energy availability in eukaryotes [1,2,3]. 8 (LST8), while differ from two representative regulatory subunits, regulatory-associated protein of mTOR (RAPTOR) and rapamycin-insensitive companion of mTOR (RICTOR), which participate in formation of TORC1 and TORC2, respectively [2,4]. Previous works show that some canonical downstream components of TOR signaling are conserved in plants, such as the ribosomal protein S6 kinase (S6K), which was reported to activate protein synthesis by phosphorylating ribosomal S6 proteins (RPS6), and the Type 2A phosphatase-associated protein of 46 kDa (TAP46), which regulates cell growth in coordination with nutrient and environmental conditions as well as the repression of programmed cell death or senescence [12,13,14]

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