Mutual antagonism of ethylene and jasmonic acid regulates ozone-induced spreading cell death in Arabidopsis. Tuominen, H., Overmyer, K., Keinänen, M., Kollist, H., & Kangasjärvi, J. The Plant Journal, 39(1):59–69, 2004. _eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-313X.2004.02107.x![Mutual antagonism of ethylene and jasmonic acid regulates ozone-induced spreading cell death in Arabidopsis [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex Ethylene (ET) and jasmonic acid (JA) have opposite effects on ozone (O3)-induced spreading cell death; ET stimulates, and is required for the spreading cell death, whereas JA protects tissues. We studied the underlying molecular mechanisms with the O3-sensitive, JA-insensitive jasmonate resistant 1 (jar1), and the O3-tolerant, ET-insensitive ethylene insensitive 2 (ein2) mutants. Blocking ET perception pharmacologically with norbornadiene (NBD) in jar1, or ET signaling genetically in the jar1 ein2 double mutant prevented the spread of cell death. This suggests that EIN2 function is epistatic to JAR1, and that the JAR1-dependent JA pathway halts oxidative cell death by directly inhibiting ET signaling. JAR1-dependent suppression of the ET pathway was apparent also as increased EIN2-dependent gene expression and ET hypersensitivity of jar1. Physiological experiments suggested that the target of JA is upstream of Constitutive Triple Response 1 (CTR1), but downstream of ET biosynthesis. Gene expression analysis of 1-aminocyclopropane-1-carboxylic acid (ACC)-treated and O3-exposed ein2 and jar1 revealed reciprocal antagonism: the EIN2-mediated suppression of the JA pathway. The results imply that the O3-induced spreading cell death is stimulated by early, rapid accumulation of ET, which can suppress the protecting function of JA thereby allowing cell death to proceed. Extended spreading cell death induces late accumulation of JA, which inhibits the propagation of cell death through inhibition of the ET pathway.
@article{tuominen_mutual_2004,
title = {Mutual antagonism of ethylene and jasmonic acid regulates ozone-induced spreading cell death in {Arabidopsis}},
volume = {39},
issn = {1365-313X},
url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-313X.2004.02107.x},
doi = {10/ft54t9},
abstract = {Ethylene (ET) and jasmonic acid (JA) have opposite effects on ozone (O3)-induced spreading cell death; ET stimulates, and is required for the spreading cell death, whereas JA protects tissues. We studied the underlying molecular mechanisms with the O3-sensitive, JA-insensitive jasmonate resistant 1 (jar1), and the O3-tolerant, ET-insensitive ethylene insensitive 2 (ein2) mutants. Blocking ET perception pharmacologically with norbornadiene (NBD) in jar1, or ET signaling genetically in the jar1 ein2 double mutant prevented the spread of cell death. This suggests that EIN2 function is epistatic to JAR1, and that the JAR1-dependent JA pathway halts oxidative cell death by directly inhibiting ET signaling. JAR1-dependent suppression of the ET pathway was apparent also as increased EIN2-dependent gene expression and ET hypersensitivity of jar1. Physiological experiments suggested that the target of JA is upstream of Constitutive Triple Response 1 (CTR1), but downstream of ET biosynthesis. Gene expression analysis of 1-aminocyclopropane-1-carboxylic acid (ACC)-treated and O3-exposed ein2 and jar1 revealed reciprocal antagonism: the EIN2-mediated suppression of the JA pathway. The results imply that the O3-induced spreading cell death is stimulated by early, rapid accumulation of ET, which can suppress the protecting function of JA thereby allowing cell death to proceed. Extended spreading cell death induces late accumulation of JA, which inhibits the propagation of cell death through inhibition of the ET pathway.},
language = {en},
number = {1},
urldate = {2021-06-15},
journal = {The Plant Journal},
author = {Tuominen, Hannele and Overmyer, Kirk and Keinänen, Markku and Kollist, Hannes and Kangasjärvi, Jaakko},
year = {2004},
note = {\_eprint: https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-313X.2004.02107.x},
keywords = {antagonism, ethylene, hormonal interactions, jasmonic acid, oxidative stress, ozone},
pages = {59--69},
}
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Blocking ET perception pharmacologically with norbornadiene (NBD) in jar1, or ET signaling genetically in the jar1 ein2 double mutant prevented the spread of cell death. This suggests that EIN2 function is epistatic to JAR1, and that the JAR1-dependent JA pathway halts oxidative cell death by directly inhibiting ET signaling. JAR1-dependent suppression of the ET pathway was apparent also as increased EIN2-dependent gene expression and ET hypersensitivity of jar1. Physiological experiments suggested that the target of JA is upstream of Constitutive Triple Response 1 (CTR1), but downstream of ET biosynthesis. Gene expression analysis of 1-aminocyclopropane-1-carboxylic acid (ACC)-treated and O3-exposed ein2 and jar1 revealed reciprocal antagonism: the EIN2-mediated suppression of the JA pathway. 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