Inositol Pyrophosphate lnsP8 Acts as an Intracellular Phosphate Signal in Arabidopsis

The maintenance of cellular phosphate(Pi)homeostasis is of great importance in living organisms.The SPX domain-containing protein 1(SPX1)proteins from both Arabidopsis and rice have been proposed to act as sensors of Pi status.The molecular signal indicating the cellular Pi status and regulating Pi homeostasis in plants,however,remains to be identified,as Pi itself does not bind to the SPX domain.Here,we report the identification of the inositol pyrophosphate lnsP8 as a signaling molecule that regulates Pi homeostasis in Arabidopsis.Polyacrylamide gel electrophoresis profiling of InsPs revealed that lnsP8 level positively cor­relates with cellular Pi concentration.We demonstrated that the homologs of diphosphoinositol pentaki-sphosphate kinase(PPIP5K),VIH1 and VIH2,function redundantly to synthesize lnsP8,and that the vih1 vih2 double mutant overaccumulates Pi.SPX1 directly interacts with PHR1,the central regulator of Pi star­vation responses,to inhibit its function under Pi-replete conditions.However,this interaction is compro­mised in the vih1 vih2 double mutant,resulting in the constitutive induction of Pi starvation-induced genes,indicating that plant cells cannot sense cellular Pi status without lnsP8.Furthermore,we showed that lnsP8 could directly bind to the SPX domain of SPX1 and is essential for the interaction between SPX1 and PHR1.Collectively,our study suggests that lnsP8 is the intracellular Pi signaling molecule serving as the ligand of SPX1 for controlling Pi homeostasis in plants.

The chromatin remodeler BRAHMA recruits HISTONE DEACETYLASE6 to regulate root growth inhibition in response to phosphate starvation in Arabidopsis

Plasticity in root system architecture(RSA)allows plants to adapt to changing nutritional status in the soil.Phosphorus availability is a major determinant of crop yield,and RSA remodeling is critical to increasing the efficiency of phosphorus acquisition.Although substantial progress has been made in understanding the signaling mechanism driving phosphate starvation responses in plants,whether and how epigenetic regulatory mechanisms contribute is poorly understood.Here,we report that the Switch defective/sucrose non-fermentable(SWI/SNF)ATPase BRAHMA(BRM)is involved in the local response to phosphate(Pi)starvation.The loss of BRM function induces iron(Fe)accumulation through increased LOW PHOSPHATE ROOT1(LPR1)and LPR2 expression,reducing primary root length under Pi deficiency.We also demonstrate that BRM recruits the histone deacetylase(HDA)complex HDA6-HDC1 to facilitate histone H3 deacetylation at LPR loci,thereby negatively regulating local Pi deficiency responses.BRM is degraded under Pi deficiency conditions through the 26 S proteasome pathway,leading to increased histone H3 acetylation at the LPR loci.Collectively,our data suggest that the chromatin remodeler BRM,in concert with HDA6,negatively regulates Fe-dependent local Pi starvation responses by transcriptionally repressing the RSA-related genes LPR1 and LPR2 in Arabidopsis thaliana.