GDSL lipase 1 regulates ethylene signaling and ethylene‐associated systemic immunity in Arabidopsis
pmid: 24631536
GDSL lipase 1 regulates ethylene signaling and ethylene‐associated systemic immunity in Arabidopsis
Arabidopsis GDSL lipase 1 (GLIP1) has been shown to modulate systemic immunity through the regulation of ethylene signaling components. Here we demonstrate that the constitutive triple response mutant ctr1‐1 requires GLIP1 for the ethylene response, gene expression, and pathogen resistance. The glip1‐1 mutant was defective in induced resistance following primary inoculation of necrotrophic pathogens, whereas GLIP1‐overexpressing plants showed resistance to multiple pathogens. Necrotrophic infection triggered the downregulation of EIN3 and the activation of ERF1 and SID2 in a GLIP1‐dependent manner. These results suggest that GLIP1 positively and negatively regulates ethylene signaling, resulting in an ethylene‐associated, necrotroph‐induced immune response.
- Korea University Korea (Republic of)
- Korea University Korea (Republic of)
- Korea Basic Science Institute Korea (Republic of)
- Korea University Japan
- The Korea Basic Science Institute (KBSI)
GLIP1, Arabidopsis, Gene Expression, Pseudomonas syringae, Ethylene, ERF1, Plant Growth Regulators, Gene Expression Regulation, Plant, Systemic immunity, Intramolecular Transferases, Disease Resistance, Plant Diseases, EIN3, Base Sequence, Arabidopsis Proteins, Nuclear Proteins, Salicylic acid, Sequence Analysis, DNA, Ethylenes, DNA-Binding Proteins, Plant Leaves, Host-Pathogen Interactions, Carboxylic Ester Hydrolases, Peptide Termination Factors, Signal Transduction, Transcription Factors
GLIP1, Arabidopsis, Gene Expression, Pseudomonas syringae, Ethylene, ERF1, Plant Growth Regulators, Gene Expression Regulation, Plant, Systemic immunity, Intramolecular Transferases, Disease Resistance, Plant Diseases, EIN3, Base Sequence, Arabidopsis Proteins, Nuclear Proteins, Salicylic acid, Sequence Analysis, DNA, Ethylenes, DNA-Binding Proteins, Plant Leaves, Host-Pathogen Interactions, Carboxylic Ester Hydrolases, Peptide Termination Factors, Signal Transduction, Transcription Factors
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