Plants have evolved an array of adaptive responses to low Pi availability, a process modulated by various external stimuli and endogenous growth regulatory signals. Little is known about how these signaling processes interact to produce an integrated response. Arabidopsis thaliana PHOSPHATE STARVATION RESPONSE1 (PHR1) encodes a conserved MYB-type transcription factor that is essential for programming Pi starvation-induced gene expression and downstream Pi starvation responses (PSRs). Here, we show that loss-of-function mutations in FHY3 and FAR1, encoding two positive regulators of phytochrome signaling, and in EIN3, encoding a master regulator of ethylene responses, cause attenuated PHR1 expression, whereas mutation in HY5, encoding another positive regulator of light signaling, causes increased PHR1 expression. FHY3, FAR1, HY5, and EIN3 directly bind to the PHR1 promoter through distinct cis-elements. FHY3, FAR1, and EIN3 activate, while HY5 represses, PHR1 expression. FHY3 directly interacts with EIN3, and HY5 suppresses the transcriptional activation activity of FHY3 and EIN3 on PHR1 Finally, both light and ethylene promote FHY3 protein accumulation, and ethylene blocks the light-promoted stabilization of HY5. Our results suggest that light and ethylene coordinately regulate PHR1 expression and PSRs through signaling convergence at the PHR1 promoter.
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