The remodeling of root architecture is a major developmental response of plants to phosphate (Pi) deficiency and is thought to enhance a plant’s ability to forage for the available Pi in topsoil.The underlying mechanism controlling this response,however,is poorly understood.In this study,we identified an Arabidopsis mutant,hpsl0 (hypersensitive to Pi starvation 10),which is morphologically normal under Pi sufficient condition but shows increased inhibition of primary root growth and enhanced production of lateral roots under Pi deficiency,hpsl0 is a previously identified allele (als3-3) of the ALUMINUM SENSITIVE3 (ALS3) gene,which is involved in plant tolerance to aluminum toxicity.Our results show that ALS3 and its interacting protein AtSTAR1 form an ABC transporter complex in the tonoplast.This protein complex mediates a highly electrogenie transport in Xenopus oocytes.Under Pi deficiency,als3 accumulates higher levels of Fe3+ in its roots than the wild type does.In Arabidopsis,LPR1 (LOW PHOSPHATE ROOT1) and LPR2 encode ferroxidases,which when mutated,reduce Fe3+ accumulation in roots and cause root growth to be insensitive to Pi deficiency.Here,we provide compelling evidence showing that ALS3 cooperates with LPR1/2 to regulate Pi deficiency-induced remodeling of root architecture by modulating Fe homeostasis in roots.