The RLK7-MPK3/6-LEAFY PETIOLE signaling axis mediates growth inhibition during PIP peptide-induced immunity in Arabidopsis

Pathogen-associated molecular patterns (PAMPs) activate plant immunity through plasma membrane-localized receptor-like kinases (RLKs) and receptor-like proteins. The PAMP flg22 binds FLAGELLIN SENSING 2 (FLS2), inducing the expression of defense-related genes, including PAMP-INDUCED PEPTIDEs (PIPs), which enhance pathogen resistance via RLK7. However, the mechanisms underlying PAMP- and PIP-mediated growth-defense trade-off remain unclear. Here, we show that PIP1 and PIP2 suppress lateral root (LR) development and seedling growth through the RLK7-MPK3/6-LEAFY PETIOLE (LEP) signaling cascade, with LEP acting as a key node inhibiting LR formation and seedling growth. Exogenous application of PIP1/2 peptides and overexpression of prePIP1and prePIP2 inhibited LR development, while mutations in prePIP1 or prePIP2 enhanced primary root growth and accelerated LR kinetics. Genetic analyses, coimmunoprecipitation, peptide-binding and kinase assays, rapamycin-induced dimerization, and a BIR3 chimera system collectively revealed that PIP1/2 recognition promoted RLK7 interaction with SOMATIC EMBRYOGENESIS RECEPTOR KINASE coreceptors, triggering MPK3/6-dependent phosphorylation events that inhibit LR development. The transcription factor LEP acted downstream of the RLK7-MPK6, inhibiting LR development. Loss of LEP function alleviated PIP-induced inhibition of seedling growth and LR formation without compromising immune responses. These findings suggest that PIP1/2 mediate the trade-off between growth and defense via the RLK7-MPK6-LEP signaling axis. The flg22 peptide suppressed LR formation and seedling growth in part through the PIP1/2-RLK7-MPK6-LEP signaling pathway bifurcating from immune responses downstream of MPK3/6. This study established a genetic framework for optimizing crop resilience by decoupling immune activation from growth suppression.