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Ambient temperature induces the hypocotyl elongation of seedling, called as thermomorphogenesis. It has been reported that the bHLH transcriptional factor PIF7 acts as the critical component to modulate plant thermomorphogenesis, but the underlying mechanism remains elusive. The phytohormone abscisic acid (ABA) suppresses the hypocotyl elongation under high temperature (HT) stress. As the ABI5 binding protein, AFP2 acts as the negative factor to control ABA signaling. In this study, we first identified AFP2 as the interaction protein of PIF7  in vitro  and  in vivo . Phenotype analysis revealed that overexpressing  AFP2  reduced the hypocotyl elongation, while loss-of-function  afp2  mutant showed longer hypocotyl under HT. Consistently, overexpressing  AFP2  impaired the transactivation effect of PIF7 on auxin biosynthesis related genes  YUC8  and  IAA19 , which possibly resulted into the shorter hypocotyl in the transgenic line overexpressing  AFP2  or co-overexpressing  AFP2  and  PIF7 . Thus, these data suggest that AFP2 suppressed PIF7 activity to suppress hypocotyl elongation. Furthermore, we found that HT gradually induced the degradation of AFP2 that possibly released the inhibitory effect of AFP2 on PIF7, thus induced hypocotyl elongation under HT. Taken together, our result reveals the novel function of AFP2 in coordinating thermomorphogenesis through sophistically modulating PIF7 activity.

AFP2 Coordinates the Activity of PIF7 for Thermomorphogenesis in Arabidopsis Seedlings