ArticlePlant communications2026
The RLK7-MPK3/6-LEAFY PETIOLE signaling axis mediates growth inhibition during PIP peptide-induced immunity in Arabidopsis.
Article in Plant communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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 those encoding 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 that inhibits LR formation and seedling growth. Exogenous application of PIP1/2 peptides and overexpression of prePIP1 and prePIP2 inhibit LR development, whereas mutations in prePIP1 or prePIP2 enhance primary root growth and accelerate LR develomental kinetics. Genetic analyses, coimmunoprecipitation, peptide-binding and kinase assays, rapamycin-induced dimerization, and a BIR3 chimera system collectively revealed that PIP1/2 recognition promotes the interaction of RLK7 with SOMATIC EMBRYOGENESIS RECEPTOR KINASE coreceptors, triggering MPK3/6-dependent phosphorylation events and inhibiting LR development. The transcription factor LEP acts downstream of RLK7-MPK6 signaling to inhibit LR development. Loss of LEP function alleviates PIP-induced inhibition of seedling growth and LR formation without compromising immune responses. These findings suggest that PIP1/2 peptides mediate the trade-off between growth and defense via the RLK7-MPK6-LEP signaling axis. The flg22 peptide suppresses LR formation and seedling growth in part through the PIP1/2-RLK7-MPK6-LEP signaling pathway, which bifurcates from immune responses downstream of MPK3/6. This study establishes a genetic framework for optimizing crop resilience by decoupling immune activation from growth suppression.
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