Abstract
Leaf senescence is induced by various internal and external stimuli. Dark-induced senescence has been extensively investigated, but the detailed mechanism underlying it is not well understood. The red light/far-red light receptor phytochrome B and its downstream transcription factors, PYHTOCHROME INTERACTING FACTORs (PIFs) 4 and 5, are known to play an important role in dark-induced senescence. Furthermore, the senescence-inducing phytohormones, ethylene and abscisic acid (ABA) are reported to be involved in dark-induced senescence. In this study, we analyzed the relationship between ethylene, ABA and PIFs in dark-induced leaf senescence. A triple mutant of the core ABA signaling components; SNF1-related protein kinases 2D (SRK2D), SRK2E, and SRK2I, displayed an ABA insensitive phenotype in ABA-induced senescence, whilst the ethylene insensitive mutant ein2 demonstrated low sensitivity to ABA, suggesting that ethylene signaling is involved in ABA-induced senescence. However, the pif4 pif5 mutant did not display low sensitivity to ABA, suggesting that PIF4 and PIF5 act upstream of ABA signaling. Although PIF4 and PIF5 reportedly regulate ethylene production, the triple mutant ein2 pif4 pif5 showed a stronger delayed senescence phenotype than ein2 or pif4 pif5, suggesting that EIN2 and PIF4/PIF5 partially regulate leaf senescence independently of each other. While direct target genes for PIF4 and PIF5, such as LONG HYPOCOTYL IN FAR-RED1 (HFR1) and PHYTOCHROME INTERACTING FACTOR 3-LIKE 1 (PIL1), showed transient upregulation under dark conditions (as is seen in the shade avoidance response), expression of STAY GREEN1 (SGR1), ORESARA1 (ORE1) and other direct target genes of PIF5, continued to increase during dark incubation. It is possible that transcription factors other than PIF4 and PIF5 are involved in the upregulation of SGR1 and ORE1 at a later stage of dark-induced senescence. Possible candidates are senescence-induced senescence regulators (SIRs), which include the NAC transcription factors ORE1 and AtNAP. In fact, ORE1 is known to bind to the SGR1 promoter and promotes its expression. It is therefore inferred that the phytochrome-PIF pathway regulates initial activation of senescence and subsequently, induced SIRs reinforce leaf senescence during dark-induced senescence.
Highlights
Leaf senescence is a system to recover nutrients from unnecessary leaves, which is accompanied by drastic changes in metabolism, gene expression and cell structure
Expression of DIN6, a marker gene for sugar starvation (BaenaGonzález et al, 2007), was drastically upregulated in the darktreated mock condition, but this upregulation was repressed by 50 mM glucose treatment, suggesting that repression of sugar starvation could not fully repress dark-induced leaf senescence
We investigated the genetic interaction between ethylene signaling and PIF4/PIF5 in dark-induced senescence. pif4 pif5 shows a delayed senescence phenotype, but the 7th leaf turned completely yellow under dark conditions at 14 days after the start of treatment (DAT) (Figures 4A,B). ein2-5 showed a stronger delayed senescence phenotype, with the 7th leaf remaining green at 14 DAT and tuning yellow at 18 DAT
Summary
Leaf senescence is a system to recover nutrients from unnecessary leaves, which is accompanied by drastic changes in metabolism, gene expression and cell structure. By internal factors such as aging and flowering, and by various external stimuli such as prolonged dark incubation, drought, and salinity (Schippers, 2015). The ABA signaling transcription factors ABA INSENSITIVE5 (ABI5) and ENHANCED EM LEVEL (EEL) are reportedly involved in leaf senescence (Sakuraba et al, 2014). Further phytohormones such as jasmonic acid (Zhuo et al, 2020) and salicylic acid (Yoshimoto et al, 2009) are known to be involved in leaf senescence. The senescence promoting function of strigolactone is strongly associated with ethylene signaling (Ueda and Kusaba, 2015)
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