Abstract
The cpr5-1 Arabidopsis thaliana mutant exhibits constitutive activation of salicylic acid (SA), jasmonic acid (JA) and ethylene (ET) signalling pathways and displays enhanced tolerance of heat stress (HS).
cpr5-1 crossed with jar1-1 (a JA-amino acid synthetase) was compromised in basal thermotolerance, as were the mutants opr3 (mutated in OPDA reductase3) and coi1-1 (affected in an E3 ubiquitin ligase F-box; a key JA-signalling component). In addition, heating wild-type Arabidopsis led to the accumulation of a range of jasmonates: JA, 12-oxophytodienoic acid (OPDA) and a JA-isoleucine (JA-Ile) conjugate. Exogenous application of methyl jasmonate protected wild-type Arabidopsis from HS.
Ethylene was rapidly produced during HS, with levels being modulated by both JA and SA. By contrast, the ethylene mutant ein2-1 conferred greater thermotolerance.
These data suggest that JA acts with SA, conferring basal thermotolerance while ET may act to promote cell death.
cpr5-1 crossed with jar1-1 (a JA-amino acid synthetase) was compromised in basal thermotolerance, as were the mutants opr3 (mutated in OPDA reductase3) and coi1-1 (affected in an E3 ubiquitin ligase F-box; a key JA-signalling component). In addition, heating wild-type Arabidopsis led to the accumulation of a range of jasmonates: JA, 12-oxophytodienoic acid (OPDA) and a JA-isoleucine (JA-Ile) conjugate. Exogenous application of methyl jasmonate protected wild-type Arabidopsis from HS.
Ethylene was rapidly produced during HS, with levels being modulated by both JA and SA. By contrast, the ethylene mutant ein2-1 conferred greater thermotolerance.
These data suggest that JA acts with SA, conferring basal thermotolerance while ET may act to promote cell death.
Original language | English |
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Pages (from-to) | 175-187 |
Number of pages | 13 |
Journal | New Phytologist |
Volume | 182 |
Issue number | 1 |
DOIs | |
Publication status | Published - Apr 2009 |
Keywords
- MUSTARD SEEDLINGS
- RESPONSE PATHWAYS
- PLANT DEFENSIN GENE
- METHYL JASMONATE
- DEPENDENT CELL-DEATH
- INDUCED RESISTANCE
- TEMPERATURE STRESS
- SIGNALING PATHWAYS
- REGULATED DEFENSE
- INDUCED GENE-EXPRESSION