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The Arabidopsis hrl1 mutation reveals novel overlapping roles for salicylic acid, jasmonic acid and ethylene signalling in cell death and defence against pathogens
Author(s) -
Devadas Sendil K.,
Enyedi Alexander,
Raina Ramesh
Publication year - 2002
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1046/j.1365-313x.2002.01300.x
Subject(s) - jasmonic acid , biology , pseudomonas syringae , hypersensitive response , arabidopsis , npr1 , salicylic acid , mutant , programmed cell death , arabidopsis thaliana , microbiology and biotechnology , gene expression , plant disease resistance , gene , biochemistry , pathogen , apoptosis , medicine , heart failure , natriuretic peptide
Summary Defence against pathogens in Arabidopsis is orchestrated by at least three signalling molecules: salicylic acid (SA), jasmonic acid (JA) and ethylene (ET). The hrl1 ( hypersensitive response‐like lesions 1 ) mutant of Arabidopsis is characterized by spontaneous necrotic lesions, accumulation of reactive oxygen species, constitutive expression of SA‐ and ET/JA‐responsive defence genes, and enhanced resistance to virulent bacterial and oomycete pathogens. Epistasis analyses of hrl1 with npr1 , etr1, coi1 and SA‐depleted nahG plants revealed novel interactions between SA and ET/JA signalling pathways in regulating defence gene expression and cell death. RNA gel‐blot analysis of RNA isolated separately from the lesion + and the lesion – leaves of double mutants of hrl1 revealed different signalling requirements for the expression of defence genes in these tissues. Expression of the ET/JA‐responsive PDF1.2 gene was markedly reduced in hrl1 npr1 and in SA‐depleted hrl1 nahG plants. In hrl1 nahG plants, expression of PDF1.2 was regulated by benzathiadiazole in a concentration‐dependent manner: induced at low concentration and suppressed at high concentration. The hrl1 etr1 plants lacked systemic PR‐1 expression, and exhibited compromised resistance to virulent Pseudomonas syringae and Peronospora parasitica . Inhibiting JA responses in hrl1 coi1 plants lead to exaggerated cell death and severe stunting of plants. Finally, the hrl1 mutation lead to elevated expression of AtrbohD , which encodes a major subunit of the NADPH oxidase complex. Our results indicate that defence gene expression and resistance against pathogens in hrl1 is regulated synergistically by SA and ET/JA defence pathways.