Decoupling low phytic acid from growth penalties by targeting PHR1 / PHL1 in Arabidopsis

) is the primary phosphorus storage form in seeds, but its poor digestibility in monogastric animals and strong chelation of essential minerals reduce nutritional value, while undigested PA contributes to environmental eutrophication. Developing low phytic acid (LPA) crops is critical for sustainable agriculture, yet LPA genotypes typically exhibit pleiotropic growth defects that limit breeding applications. We employed a forward genetic suppressor screen to identify suppressor mutations in the Arabidopsis ipk1-1 mutant background. Suppressor lines were characterized through mapping-by-sequencing, complementation analysis, and phenotypic assessment including phosphate quantification, gene expression profiling and phytic acid measurement. We discovered that LPA triggers constitutive activation of the phosphate starvation response (PSR), leading to excessive phosphate accumulation and elevated salicylic acid (SA) biosynthesis that drives premature leaf senescence. Loss-of-function mutations in PHR1/PHL1 block this hyperactive signalling cascade, normalizing SA levels and suppressing senescence-associated gene expression while maintaining the low phytic acid phenotype. Our findings provide independent genetic evidence, obtained through a forward suppressor screen, that loss of PHR1/PHL1 function blocks the aberrant PSR and SA accumulation triggered by IPK1 deficiency, thereby preventing premature senescence while maintaining the LPA phenotype. This work extends the established framework of PHR1/PHL1-dependent signalling to include seed yield, germination, and senescence, offering a refined strategy for developing low phytic acid crops with minimal agronomic penalties.