BBX24 interacts with JAZ3 to promote growth by reducing DELLA activity in shade avoidance.

Shade avoidance syndrome (SAS) is a strategy of major adaptive significance and typically includes elongation of the stem and petioles, leaf hyponasty, reduced branching, and phototropic orientation of the plant shoot toward canopy gaps. Cryptochrome 1 and phytochrome B (phyB) are both the major photoreceptors that sense the reduction in blue light fluence rate and the low Red:Far-Red (R:FR) ratio, respectively, both light signals associated with plant density and the resource reallocation when SAS responses are triggered. BBX24 has been implicated in the SAS as a regulator of DELLA activity, but this interaction does not explain all the observed BBX24-dependent regulation in shade light. Here, through a combination of transcriptional meta-analysis and large-scale identification of BBX24-interacting transcription factors, we found that JAZ3, a jasmonic acid signaling component, is a direct target of BBX24. Furthermore, we demonstrated that joint loss of BBX24 and JAZ3 function causes insensitivity to DELLA accumulation, and the defective shade-induced elongation in this mutant is rescued by loss of DELLA or phytochrome B functions. Therefore, we propose that JAZ3 is part of the regulatory network that controls the plant growth in response to shade, through a mechanism in which BBX24 and JAZ3 jointly regulate DELLA activity. Our results provide new insights into the participation of BBX24 and JA signaling in the hypocotyl shade avoidance response in Arabidopsis.