Seedlings respond to ambient temperature through thermomorphogenesis, characterised by elongation of the hypocotyl (embryonic stem) and petiole with hynonastic growth. PHYTOCHROME INTERCTING FACTOR 4 (PIF4) is a known key regulator of thermomorphogenesis; however, the underlying molecular mechanisms remain unclear. Now, Enamul Huq and colleagues reveal that SUPPRESSOR OF PHYA-105 (SPA) genes are required for thermomorphogenesis in Arabidopsis. Ablation of all four SPA genes in spaQ mutants prevents thermomorphogenesis in seedlings grown at 28°C, which is partially rescued by ectopic SPA1 expression. Transcriptome analyses reveal that spaQ mutants share over 30% of differentially regulated genes with pif4 mutants, suggesting a common mechanism. Indeed, the authors show that SPAs promote PIF4 stability in vivo, and that SPA1 directly phosphorylates PIF4 in vitro. Supporting this, expression of a SPA1 mutant protein without the kinase activity fails to rescue the spaQ mutant phenotype or stabilise phosphorylated PIF4. Finally, the researchers suggest that SPAs regulate the degradation of the temperature sensor phytochrome B (phyB), and show that SPA, phyB and PIF4 can form a complex in vitro. Taken together, these data indicate that SPAs regulate thermomorphogenesis by promoting PIF4 stability through direct phosphorylation and provide new insights into this mechanism.
