PHR1 and PHL1 mediate rapid high-light responses and acclimation to high photosynthetic activity

Abstract

O_LIRapid acclimation towards high light is vital for the prevention of phototoxic stress to plant tissues. Photosynthesis transiently consumes inorganic phosphate (Pi). We therefore asked whether changes in intracellular Pi pools can act as a signal for reprogramming gene expression upon increased light intensity. C_LIO_LIThe function of triose phosphate utilization for intracellular Pi homeostasis was deciphered by investigation of mutants defective in both photoassimilate partitioning and low-Pi signaling. Next, we determined subcellular Pi levels and transcript accumulation upon short-term high light. Physiological consequences were examined by analyses of ATP, carbohydrates, and an untargeted lipid profiling approach. C_LIO_LIThe capacity for triose phosphate utilization clearly affected systemic Pi signaling. High-light treatment caused a rapid depletion specifically of chloroplast Pi levels paralleled by induction of transcripts dependent on PHOSPHATE STARVATION RESPONSE 1 (PHR1) and PHR1-LIKE 1. Among the high-light induced targets of PHR1, SRG3/GDPD1 is involved in phospholipid catabolism. Lipid profiling revealed differences between WT and srg3 mutant plants upon high light, including changes in linolenic acid and photoprotective zeaxanthin. C_LIO_LIWe conclude that photosynthetic activity regulates the low-Pi response machinery in the nucleus to implement high-light acclimation. This facilitates the liberation of cellular P as well as the maintenance of membrane lipid integrity. C_LI