Iron-dependent reprogramming of damage-associated peptide receptor signaling coordinates immunity and phosphate stress adaptation

Abstract Plant adaptation to inorganic phosphate (Pi) limitation entails extensive developmental and metabolic reprogramming, collectively termed the phosphate starvation response (PSR). How plants balance nutrient acquisition with immune competence remains unresolved. Here, we show that PSR reconfigures the immune receptor landscape in Arabidopsis thaliana, selectively retaining multifunctional damage-associated molecular pattern (DAMP) receptors. Membrane proteomics revealed increased abundance of the Pep receptor PEPR1 under Pi deficiency, whereas most receptor kinases, including microbial pattern-recognition receptors such as FLS2 and CERK1, are reduced. Consistently, Pep-triggered responses are strongly potentiated under Pi depletion, while flagellin- and chitin-induced responses are not, indicating receptor-level immune pathway prioritization rather than global suppression. Mechanistically, Pep sensitization requires the PSR-related ferroxidases LPR1/LPR2, NADPH oxidases RBOHD/RBOHF, and transcription factor WRKY33, linking iron-dependent redox remodeling to selective immune amplification. Beyond inducible defense, PEPRs promote basal PSR transcriptional reprogramming and growth under Pi limitation. Loss of PEPR1/PEPR2 compromises bacterial resistance and alters root-associated microbiota composition under nutrient deficiency. Together, our findings indicate that specific DAMP receptors exhibit context-dependent dual functionality, promoting immunity or nutrient stress adaptation under Pi depletion, sustaining immune vigilance while optimizing nutrient acquisition. This receptor-level prioritization provides a framework for how nutritional status reshapes plant innate immune architecture. Competing Interest Statement The authors have declared no competing interest.