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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

ABSTRACT: 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.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE136268 | GEO | 2021/07/15

REPOSITORIES: GEO

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Project description:As sessile organism, plants evolved a highly complicated signaling system to cope with unfavorable and fluctuating environmental conditions. Rapid and transient Reactive Oxygen Species (ROS) burst is a common response to both biotic and abiotic stresses. Plants exposed with O3 could trigger extracellular similar ROS production through cell wall peroxidases and NPADPH oxidases, resulting in changes in the gene expression and cell death. Whereas ROS induced cell death is not simply due to its toxicity, rather due to interplay with several other signaling pathways, such as salicylic acid (SA), jasmonic acid (JA) and ethylene signaling pathways. Furthermore, the three hormones have both synergistic and antagonistic interactions, where the suppression of JA signaling by SA is the mostly studied. In addition, ethylene promotes cell death while JA has a protective role upon O3 exposure. The role of SA is more complicated; depending on the genetic background it can have either cell death promoting or protecting roles. Hence, a clean system to deliver apoplastic ROS is required to study the role of ROS apart from con-current activation of other signaling pathways. Arabidopsis thaliana offer a convenient system to study apoplastic ROS signaling due to the availability of hormone signaling or biosynthesis mutants including the JA receptor mutant coi1-16 (CORONATINE INSENSITIVE1), the essential ethylene signaling mutant ein2 (ETHYLENE INSENSITIVE2), the SA biosynthesis mutant sid2 (SALICYLIC ACID INDUCTION DEFICIENT2 also known as ISOCHORISMATE SYNTHASE1), and essential regulators in SA/JA/ethylene-induced defense response triple mutant tga2 tga5 tga6 (Clade II TGA transcription factors). Here we used a combination of transcriptome analysis, cell death assays and mutant analysis to systematically quantified the contribution of hormone signaling in relation to apoplastic ROS signaling, identified transcription factors (TFs) involved in ROS regulation and dissected the components involved in defense hormones associated cell death. Transcriptome profiling of ozone response using two arabidopsis triple mutants coi1-16 ein2 sid2 and tga2 tga5 tga6 related to Jasmonic acid, salicylic acid and ethylene signaling to identify hormone-independant apoplastic ROS signaling