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Plant J. 2019 Sep 30. doi: 10.1111/tpj.14556. [Epub ahead of print]

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

Author information

1
Department of Botany and Plant Biology, Section of Biology, Faculty of Science, University of Geneva, CH-1211, Geneva 4, Switzerland.
2
Institute of Genetics and Genomics of Geneva (iGE3), University of Geneva, Geneva, Switzerland.

Abstract

Hypocotyl growth inhibition 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 hypocotyl growth inhibition 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 as well. However, here we demonstrate that hy5 hyh double mutants maintain significant UVR8-dependent hypocotyl growth inhibition. We identify UVR8-dependent inhibition of the bHLH transcription factors PHYTOCHROME INTERACTING FACTOR 4 (PIF4) and PIF5 activities as part of the UVR8 signaling pathway, which results in hypocotyl growth inhibition. UVR8-mediated repression of several hypocotyl elongation-related genes is independent of HY5 and HYH but largely associated with UVR8-dependent PIF4 and PIF5 degradation, 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 PIFs function as integrators of different photoreceptor signaling pathways.

KEYWORDS:

Arabidopsis thaliana ; COP1; HY5; PIF4; PIF5; UVR8; photomorphogenesis; signal transduction; ultraviolet-B

PMID:
31571300
DOI:
10.1111/tpj.14556

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