Thermomorphogenesis is the morphological response of plants to an elevation in the ambient temperature, which is mediated by the bHLH transcription factor PIF4. The evening-expressed clock component, PRR5, directly represses the expression of PIF4 mRNA. Additionally, PRR5 interacts with PIF4 protein and represses its transactivation activity, which in turn suppresses the thermoresponsive growth in the evening. Here, we found that the B-box zinc finger protein, BBX18, interacts with PRR5 through the B-Box2 domain. Deletion of the B-Box2 domain abolished the functions of BBX18, including the stimulation of PIF4 mRNA expression and hypocotyl growth. Overexpression of BBX18, and not of B-Box2-deleted BBX18, restored the expression of thermoresponsive genes in the evening. We further show that BBX18 prevents PRR5 from inhibiting PIF4-mediated high temperature responses. Taken together, our results suggest that BBX18 regulates thermoresponsive growth through the PRR5-PIF4 pathway.
Plants adapt to high temperature stresses through thermomorphogenesis, a process that includes stem elongation and hyponastic leaf growth. Thermomorphogenesis is gated by the circadian clock through two evening-expressed clock components, TIMING OF CAB EXPRESSION1 (TOC1) and PSEUDO-RESPONSE REGULA-TORS5 (PRR5). These proteins directly interact with and inhibit PHYTOCHROME INTERACTING FACTOR4 (PIF4), a basic helix-loop-helix transcription factor that promotes thermoresponsive growth. PIF4-mediated thermoresponsive growth is positively regulated by ZEITLUPE (ZTL), a central clock component, but the molecular mechanisms underlying this are poorly understood. Here, we show that ZTL regulates thermoresponsive growth through TOC1 and PRR5. Genetic analyses reveal that ZTL regulates PIF4 activity as well as PIF4 expression. In Arabidopsis thaliana, ztl mutants exhibit highly accumulated TOC1 and PRR5 and unresponsive expression of PIF4 target genes under exposure to high temperatures. Mutations in TOC1 and PRR5 restore thermoactivation of PIF4 target genes and thermoresponsive growth in ztl mutants. We also show that the molecular chaperone heat-shock protein 90 promotes thermoresponsive growth through the ZTL-TOC1/PRR5 signaling module. Further, we show that ZTL protein stability is increased at high temperatures. Taken together, our results demonstrate that ZTL-mediated degradation of TOC1 and PRR5 enhances the sensitivity of hypocotyl growth to high temperatures.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.