Phytochromes (Phy) and phytochrome-interacting factor (PIF) transcription factors constitute a major signaling module that controls plant development in response to red and far-red light. A low red:far-red ratio is interpreted as shading by neighbor plants and induces cell elongation-a phenomenon called shade-avoidance syndrome (SAS). PAR1 and its closest homolog PAR2 are negative regulators of SAS; they belong to the HLH transcription factor family that lacks a typical basic domain required for DNA binding, and they are believed to regulate gene expressions through DNA binding transcription factors that are yet to be identified. Here, we show that light signal stabilizes PAR1 protein and PAR1 interacts with PIF4 and inhibits PIF4-mediated gene activation. DNA pull-down and chromatin immunoprecipitation (ChIP) assays showed that PAR1 inhibits PIF4 DNA binding in vitro and in vivo. Transgenic plants overexpressing PAR1 (PAR1OX) are insensitive to gibberellin (GA) or high temperature in hypocotyl elongation, similarly to the pifq mutant. In addition to PIF4, PAR1 also interacts with PRE1, a HLH transcription factor activated by brassinosteroid (BR) and GA. Overexpression of PRE1 largely suppressed the dwarf phenotype of PAR1OX. These results indicate that PAR1-PRE1 and PAR1-PIF4 heterodimers form a complex HLH/bHLH network regulating cell elongation and plant development in response to light and hormones.

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