Abstract
Aging of living organisms is governed by intrinsic developmental programs, of which progression is often under the regulation of their cellular energy status. For example, calorie restriction is known to slow down aging of heterotrophic organisms from yeasts to mammals. In autotrophic plants cellular energy deprivation by perturbation of photosynthesis or sugar metabolism is also shown to induce senescence delay. However, the underlying molecular and biochemical mechanisms remain elusive. Our plant cell-based functional and biochemical assays have demonstrated that SNF1-RELATED KINASE1 (SnRK1) directly interacts, phosphorylates, and destabilizes the key transcription factor ETHYLENE INSENSITIVE3 (EIN3) in senescence-promoting hormone ethylene signaling. Combining chemical manipulation and genetic validation using extended loss-of-function mutants and gain-of-function transgenic lines, we further revealed that a SnRK1 elicitor, 3-(3,4-dichlorophenyl)-1,1-dimethylurea enables to slow down senescence-associated leaf degreening through the regulation of EIN3 in Arabidopsis. Our findings enlighten that an evolutionary conserved cellular energy sensor SnRK1 plays a role in fine-tuning of organ senescence progression to avoid sudden death during the last step of leaf growth and development.
Highlights
Plant vegetative organ senescence often accompanies reproductive and/or dormant meristematic organ formation and development[5]
In our small scale interaction screen of a>] KINASE HOMOLOG 10 (AKIN10) with several transcription factors involved in stress and hormone signaling such as MYB2, MYC2, MYC3, MYC4, JAZ and ETHYLENE INSENSITIVE3 (EIN3), we found AKIN10 interacted with MYC2 in abscisic acid and jasmonate, and EIN3 in ethylene signaling
Our RNA sequencing (RNA-seq) data analysis further identified 80 differentially expressed genes (DEG) up-regulated by both EIN3 and AKIN10 (Fig. 3e), and 146 of those down-regulated by both EIN3 and AKIN10 (Fig. 3f). Since both ethylene signaling and AKIN10 activity are reported to have a role in flooding-induced hypoxia tolerance in plants[24, 28, 29], we examined whether DEG commonly regulated by EIN3 and AKIN10 was involved in hypoxia signaling response
Summary
Plant vegetative organ senescence often accompanies reproductive and/or dormant meristematic organ formation and development[5]. In a model plant Arabidopsis ethylene signaling pathway encompasses ETHYLENE RESPONSE1 (ETR1) and four other redundant receptors that transduce the hormone signal to ETHYLENE INSENTIVIE2 (EIN2), and EIN3 and EIN3-LIKE1 (EIL1) in the nucleus[13, 14]. These key transcription factors in ethylene signaling activate specific target gene expression and their gene products involve in changes of cellular physiology. Even though ethylene is not a senescence initiation factor[19], ethylene-EIN3 signaling plays a key role in the regulation of senescence progression, any functional perturbation of EIN3 is apt to regulate plant organ senescence[20]. Its activation is triggered by hypoxia leading to suppression of mitochondrial aerobic respiration resulting in cellular energy deprivation[21, 24, 25]
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