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.
Grafting is an effective technique for increasing the resistance of vegetables to biotic and abiotic stresses. It has been widely applied to produce solanaceous and melon vegetables. Temperature is an important external factor affecting graft formation. However, the molecular mechanism by which external ambient temperature affects tomato graft formation remains unclear. In this study, we demonstrated that elevating ambient temperature during grafting to 35 °C for more than 24 h after grafting accelerated vascular reconnection. We generated self- or heterografted combinations between phyB1B2 and pif4 loss-of-function mutant and wild-type plants, and were mutants unresponsive to graft formation at elevated ambient temperature. In addition, elevated ambient temperature induced SlPIF4 expression during grafting. SlPIF4 directly binds the promoters of auxin biosynthesis genes SlYUCCA s and activates their expression. Further investigation revealed auxin accumulation in the graft junction under elevated ambient temperature. The results illuminate the mechanism by which the PHYB-PIF4-auxin module promotes tomato graft formation in response to elevated ambient temperature.
Huang Sha,Ma Yu,Xu Yitian,Lu Pengfei,Yang Jie,Xie Yu,Gan Jianhua,Li Lin
For shade-intolerant species, shade light indicates the close proximity of neighboring plants and triggers the shade avoidance syndrome (SAS), which causes exaggerated growth and reduced crop yield. Here, we report that non-secreted ROT FOUR LIKE (RTFL)/DEVIL (DVL) peptides negatively regulate SAS by interacting with BRASSINOSTEROID SIGNALING KINASEs (BSKs) and reducing the protein level of PHYTOCHROME INTERACTING FACTOR 4 (PIF4) in Arabidopsis. The transcription of at least five RTFLs ( RTFL13/16/17/18/21 ) is induced by low R:FR light. The RTFL18 (DVL1) protein is stabilized under low R:FR conditions and localized to the plasma membrane. A phenotype analysis reveals that RTFL18 negatively regulates low R:FR-promoted petiole elongation. BSK3 and BSK6 are identified as partners of RTFL18 through binding assays and structural modeling. The overexpression of RTFL18 or knockdown of BSK3/6 reduces BRASSINOSTEROID signaling and reduces low R:FR-stabilized PIF4 levels. Genetically, the overexpression of BSK3/6 and PIF4 restores the petiole phenotype acquired by RTFL18 -overexpressing lines. Collectively, our work characterizes a signaling cascade (the RTFLs-BSK3/6-PIF4 pathway) that prevents the excessive activation of the shade avoidance response in Arabidopsis.
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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