Degradation of the transcription factors PIF4 and PIF5 under UV-B promotes UVR8-mediated inhibition of hypocotyl growth in Arabidopsis.

Inhibition of hypocotyl growth is a well-established UV-B-induced photomorphogenic response that is mediated by the UV-B photoreceptor UV RESISTANCE LOCUS 8 (UVR8). However, the molecular mechanism by which UVR8 signaling triggers inhibition of hypocotyl growth is poorly understood. The bZIP protein ELONGATED HYPOCOTYL 5 (HY5) functions as the main positive regulatory transcription factor in the UVR8 signaling pathway, with HY5-HOMOLOG (HYH) playing a minor role. However, here we demonstrate that hy5 hyh double mutants maintain significant UVR8-dependent hypocotyl growth inhibition. We identify UVR8-dependent inhibition of the activities of bHLH transcription factors PHYTOCHROME INTERACTING FACTOR 4 (PIF4) and PIF5 as part of the UVR8 signaling pathway, which results in inhibition of hypocotyl growth. The UVR8-mediated repression of several hypocotyl elongation-related genes is independent of HY5 and HYH but largely associated with UVR8-dependent degradation of PIF4 and PIF5, a process that consequently diminishes PIF4/5 target promoter occupancy. Taken together, our data indicate that UVR8-mediated inhibition of hypocotyl growth involves degradation of PIF4 and PIF5. These findings contribute to our mechanistic understanding of UVR8-induced photomorphogenesis and further support the function of PIFs as integrators of different photoreceptor signaling pathways.

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