Leaf senescence can be triggered by multiple abiotic stresses including darkness, nutrient limitation, salinity, and drought. Recently, heatwaves have been occurring more frequently, and they dramatically affect plant growth and development. However, the underlying molecular networks of heat stress-induced leaf senescence remain largely uncharacterized. Here we showed that PHYTOCHROME INTERACTING FACTOR 4 (PIF4) and PIF5 proteins could efficiently promote heat stress-induced leaf senescence in Arabidopsis. Transcriptomic profiling analysis revealed that PIF4 and PIF5 are likely to function through multiple biological processes including hormone signaling pathways. Further, we characterized NAC019, SAG113, and IAA29 as direct transcriptional targets of PIF4 and PIF5. The transcription of NAC019, SAG113, and IAA29 changes significantly in daytime after heat treatment. In addition, we demonstrated that PIF4 and PIF5 proteins were accumulated during the recovery after heat treatment. Moreover, we showed that heat stress-induced leaf senescence is gated by the circadian clock, and plants might be more actively responsive to heat stress-induced senescence during the day. Taken together, our findings proposed important roles for PIF4 and PIF5 in mediating heat stress-induced leaf senescence, which may help to fully illustrate the molecular network of heat stress-induced leaf senescence in higher plants and facilitate the generation of heat stress-tolerant crops.
For shade-intolerant plants, a reduction in the red/far-red (R:FR) light ratio signals the close proximity of competitors and triggers shade-avoidance syndrome (SAS). Auxin, brassinosteroid, gibberellin and some transcriptional regulators have been reported to regulate shade-induced hypocotyl elongation. However, little is understood regarding the coordination of these multiple regulatory pathways. Here, combining time-lapse growth rates and transcriptomic data, we demonstrate that auxin and brassinosteroid affect two phases of shade-induced rapid growth, whereas gibberellin mainly contributes to the second rapid growth phase. PHYTOCHROME-INTERACTING FACTOR 7 (PIF7) acts earlier than other PIFs. PIF4 and PIF5 modulate the second rapid growth phase. LONG HYPOCOTYL IN FAR-RED 1 (HFR1) and PIF3-LIKE 1 (PIL1) modulate two rapid growth phases. Our results reveal that hormonal and transcriptional regulatory programs act together to coordinate dynamic hypocotyl changes in an immediate response to a shade signal and provide a novel understanding of growth kinetics in a changing environment.
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