Up-regulation of autophagy by low concentration of salicylic acid delays methyl jasmonate-induced leaf senescence

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 MeJAinduced leaf senescence. Collectively, our work revealed up-regulation of autophagy by LCSA as a key regulator to alleviate MeJA-induced leaf senescence. Senescence in green plants is a complex and orderly regulated process that is crucial for transiting from nutrient assimilation to nutrient remobilization 1-5. During senescence, the most visible characteristic is leaf yellowing, which is the consequence of a succession of changes in cellular physiology including chlorophyll degradation and photosynthetic activity reduction 3,4. Chloroplast as an early senescence signaling response organelle, its dismantling plays an important role in the major nitrogen source recycling and remobilization 6. The progression of leaf senescence can be prematurely induced by multiple environmental and endogenous factors, such as temperature, light, humidity and phytohormones 7. Hormone signaling pathways play roles at all the stages of leaf senescence, including the initiation, progression, and the terminal phases of senescence 7. Recent progresses show that senescence can be coordinately regulated by several phytohormones like cytokinins, ethylene, abscisic acid, salicylic acid (SA), and jasmonic acid (JA) 8-12. However, the detailed molecular mechanisms for these phytohormone signals in plant senescence remain poorly understood. JA has been known as a key plant hormone for promoting senescence, based on the findings that exogenously applied methyl jasmonate (MeJA, methyl ester of JA) leads to a rapid loss of chlorophyll content and accompany with reduction of photochemical efficiency 13,14. Studies with JA-insensitive mutant coronatine insensitive 1 (coi1) that exhibited defective senescence response to MeJA treatment 11 , supporting the notion that JA signaling pathway is crucial for leaf senescence. Some other evi...

Comparative Transcriptome-Based Mining of Senescence-Related MADS, NAC, and WRKY Transcription Factors in the Rapid-Senescence Line DLS-91 of Brassica rapa

“…This result indicates that hormones such as jasmonic acid, abscisic acid, and brassinosteroids are produced early in DLS-91—at 0 DDT, whereas salicylic acid is produced during dark treatment (1 DDT) in this genotype. Consistent with these findings, Yin et al [ 60 ] have suggested that SA delays leaf senescence by regulating concentrations of methyl jasmonates. In Arabidopsis, ABI5 has been determined to delay DLS [ 61 ].…”

Pinus pinaster Early Hormonal Defence Responses to Pinewood Nematode (Bursaphelenchus xylophilus) Infection

“…Moreover, the significant increase only in SA at 48 HAI in susceptible plants, when compared to resistant and control plants, can suggest an antagonist crosstalk between SA and JA-ME. Similarly, a negative crosstalk between SA and JA-ME has been reported in other plant defence responses [ 58 ].…”

Potential of Novel Methyl Jasmonate Analogs as Anticancer Agents to Metabolically Target HK-2 Activity in Glioblastoma Cells

“…These results indicated the presence of an undetectable cell population by Annexin-V and suggested that both cells should be evaluated for positivity of other cell death mechanisms. MJ was previously reported for its inducer role for autophagy ( Zhang et al, 2016 ; Yin et al, 2020 ). Therefore, we further focused on 24-h C-10 treatment–based enrichment of autophagy in GBM cells.…”