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A regulatory module controls plant growth and stress response by modulating hormone level

ABSTRACT: Perception and relay of cell wall signals is critical for plants to regulate growth and stress responses, but the mechanism underlying this biological process remains largely unknown. Here we report that RAPID ALKALINIZATION FACTOR (RALFs) peptides, Leucine-rich repeat extensins (LRXs) and FERONIA (FER) are physically associated in extracellular region. lrx345, fer-4, and transgenic plants overexpressing RALF22 or RALF23 all showed retarded growth, increased sensitivity to salt stress, and constitutively increased levels of ABA, JA, and SA. Salt treatment or chemical disruption of cell wall promotes the release of mature RALF peptides, which negatively regulate the function of FER by inducing its internalization. JA mutants coi1 and aos restore the retarded growth, and mutation of ABA2 suppresses the salt-sensitive phenotype of lrx345. Together, we propose that LRXs, RALFs, and FER function as a module to sense and transduce cell wall signals, thereby regulating growth and stress responses via hormones-mediated pathways.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE114682 | GEO | 2021/07/15

REPOSITORIES: GEO

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The LRX-RALF-FER cell wall integrity sensing module controls plant growth and salt stress responses by modulating multiple plant hormones

Project description:Plants have evolved cell wall integrity signaling pathways to maintain cell wall homeostasis during rapid growth and in response to environmental stress. The cell wall leucine-rich repeat extensins LRX3/4/5, the RAPID ALKALINIZATION FACTOR (RALF) peptides RALF22/23, and FERONIA (FER) function as a module to regulate plant growth and salt stress responses via the sense of cell wall integrity. However, the intracellular signaling pathways that mediate the effects of the LRX3/4/5-RALF22/23-FER module are still largely unknown. Here, we report that jasmonic acid (JA), salicylic acid (SA), and abscisic acid (ABA) accumulate constitutively in lrx345 and fer mutants. Blocking JA pathway rescues the retarded growth phenotype of the lrx345 and fer-4 mutants, while disruption of ABA biosynthesis suppresses the salt-hypersensitivity of these mutants. Many salt stress-responsive genes display abnormal expression patterns in the lrx345 and fer-4 mutants, as well as in wild type plants treated with epigallocatechin gallate (EGCG), an inhibitor of pectin methylesterases, suggesting that the cell wall integrity is a critical factor that determines the expression of stress-responsive genes. Production of reactive oxygen species (ROS) is constitutively increased in the lrx345 and fer-4 mutants, and inhibition of ROS accumulation suppresses the salt-hypersensitivity of these mutants. Together, our results suggest that the LRX3/4/5-RALF22/23-FER module controls plant growth and salt stress responses by regulating hormonal homeostasis and ROS accumulation.

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