Abstract
Light quality surrounding a plant is largely determined by the density of its neighboring vegetation. Plants are able to sense shade light signals and initiate a series of adaptation responses, which is known as shade avoidance syndrome (SAS). PHYTOCHROME INTERACTING FACTORS (PIFs) are key factors in the SAS network by regulating the biosynthesis of multiple phytohormones and the expression of cell expansion genes. Although the protein levels of PIFs were found to be acumulated in shade, the transcriptional regulation of PIFs in response to such an environmental signal remains poorly understood. Here we show that TCP17 and its two closely related homologs, TCP5 and TCP13, play an important role in mediating shade-induced hypocotyl elongation by up-regulating auxin biosynthesis via a PIF-dependent and a PIF-independent pathway. In constitutive white light, a tcp5, 13, 17 triple mutant (3tcp) showed a subtle hypocotyl defective phenotype. In shade, however, 3tcp showed a significantly reduced hypocotyl elongation phenotype, indicating a positive role of TCPs in regulating SAS. Our in-depth biochemical and genetic analyses indicated that TCP17 can be significantly accumulated in shade. TCP17 binds to the promoters of PIFs and YUCCAs to indirectly or directly up-regulate auxin levels in shade. These data provide new insights into our better understanding of the regulatory mechanisms of SAS in plants.