Abstract

Crosstalk between salicylic acid (SA) and jasmonic acid (JA) signaling plays an important role in regulation of plant senescence. Our previous work found that SA could delay methyl jasmonate (MeJA)-induced leaf senescence in a concentration-dependent manner. Here, the effect of low concentration of SA (LCSA) application on MeJA-induced leaf senescence was further assessed. High-throughput sequencing (RNA-Seq) results showed that LCSA did not have dominant effects on the genetic regulatory pathways of basal metabolism like nitrogen metabolism, photosynthesis and glycolysis. The ClusterONE was applied to identify discrete gene modules based on protein–protein interaction (PPI) network. Interestingly, an autophagy-related (ATG) module was identified in the differentially expressed genes (DEGs) that exclusively induced by MeJA together with LCSA. RT-qPCR confirmed that the expression of most of the determined ATG genes were upregulated by LCSA. Remarkably, in contrast to wild type (Col-0), LCSA cannot alleviate the leaf yellowing phenotype in autophagy defective mutants (atg5-1 and atg7-2) upon MeJA treatment. Confocal results showed that LCSA increased the number of autophagic bodies accumulated in the vacuole during MeJA-induced leaf senescence. Collectively, our work revealed up-regulation of autophagy by LCSA as a key regulator to alleviate MeJA-induced leaf senescence.

Highlights

  • Crosstalk between salicylic acid (SA) and jasmonic acid (JA) signaling plays an important role in regulation of plant senescence

  • 10 μM SA, the most effective concentration according to Ji et al.[14], was selected as low working solution to further investigate the effect of low concentration of SA (LCSA) on leaf senescence

  • These physiological and biochemical data are consistent with our previous finding that LCSA provide protection against senescence caused by methyl jasmonate (MeJA)

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Summary

Introduction

Crosstalk between salicylic acid (SA) and jasmonic acid (JA) signaling plays an important role in regulation of plant senescence. Our previous work found that SA could delay methyl jasmonate (MeJA)-induced leaf senescence in a concentration-dependent manner. The effect of low concentration of SA (LCSA) application on MeJA-induced leaf senescence was further assessed. The concentration of endogenous SA increases to upregulate several senescence-associated genes during leaf ­senescence[12,16] Such genetic regulatory mechanisms are abolished in plants defective in the SA signaling. Most of phytohormones have both stimulatory and inhibitory effects on the growth and metabolism of higher plants in a dose dependent manner It seems that SA functions in the same way on the physiological and biochemical processes of ­plants[14,19]. Based on the dose dependent effect of SA, Pasternak et al.[19] proposes that at low levels it acts as a developmental regulator and at high levels it acts as a stress h­ ormone[15]

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