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Modulation of nitrosative stress by S-nitrosoglutathione reductase is critical for thermotolerance and plant growth in Arabidopsis

Modulation of nitrosative stress by S-nitrosoglutathione reductase is critical for thermotolerance and plant growth in Arabidopsis
Modulation of nitrosative stress by S-nitrosoglutathione reductase is critical for thermotolerance and plant growth in Arabidopsis
Nitric oxide (NO) is a key signaling molecule in plants. This analysis of Arabidopsis thaliana HOT5 (sensitive to hot temperatures), which is required for thermotolerance, uncovers a role of NO in thermotolerance and plant development. HOT5 encodes S-nitrosoglutathione reductase (GSNOR), which metabolizes the NO adduct S-nitrosoglutathione. Two hot5 missense alleles and two T-DNA insertion, protein null alleles were characterized. The missense alleles cannot acclimate to heat as dark-grown seedlings but grow normally and can heat-acclimate in the light. The null alleles cannot heat-acclimate as light-grown plants and have other phenotypes, including failure to grow on nutrient plates, increased reproductive shoots, and reduced fertility. The fertility defect of hot5 is due to both reduced stamen elongation and male and female fertilization defects. The hot5 null alleles show increased nitrate and nitroso species levels, and the heat sensitivity of both missense and null alleles is associated with increased NO species. Heat sensitivity is enhanced in wild-type and mutant plants by NO donors, and the heat sensitivity of hot5 mutants can be rescued by an NO scavenger. An NO-overproducing mutant is also defective in thermotolerance. Together, our results expand the importance of GSNOR-regulated NO homeostasis to abiotic stress and plant development.
1040-4651
786-802
Lee, Ung
c945c4f2-0d65-41bf-bfbc-914cf2130afc
Wie, Chris
8792d2c0-5f29-484c-a65e-cdf2a720238c
Fernandez, Bernadette O.
27babc73-7646-4908-86e2-6c29d79fb938
Feelisch, Martin
8c1b9965-8614-4e85-b2c6-458a2e17eafd
Vierling, Elizabeth
5692b015-39be-4ee0-b40e-88f9e917afb3
Lee, Ung
c945c4f2-0d65-41bf-bfbc-914cf2130afc
Wie, Chris
8792d2c0-5f29-484c-a65e-cdf2a720238c
Fernandez, Bernadette O.
27babc73-7646-4908-86e2-6c29d79fb938
Feelisch, Martin
8c1b9965-8614-4e85-b2c6-458a2e17eafd
Vierling, Elizabeth
5692b015-39be-4ee0-b40e-88f9e917afb3

Lee, Ung, Wie, Chris, Fernandez, Bernadette O., Feelisch, Martin and Vierling, Elizabeth (2008) Modulation of nitrosative stress by S-nitrosoglutathione reductase is critical for thermotolerance and plant growth in Arabidopsis. The Plant Cell, 20 (3), 786-802. (doi:10.1105/tpc.107.052647). (PMID:18326829)

Record type: Article

Abstract

Nitric oxide (NO) is a key signaling molecule in plants. This analysis of Arabidopsis thaliana HOT5 (sensitive to hot temperatures), which is required for thermotolerance, uncovers a role of NO in thermotolerance and plant development. HOT5 encodes S-nitrosoglutathione reductase (GSNOR), which metabolizes the NO adduct S-nitrosoglutathione. Two hot5 missense alleles and two T-DNA insertion, protein null alleles were characterized. The missense alleles cannot acclimate to heat as dark-grown seedlings but grow normally and can heat-acclimate in the light. The null alleles cannot heat-acclimate as light-grown plants and have other phenotypes, including failure to grow on nutrient plates, increased reproductive shoots, and reduced fertility. The fertility defect of hot5 is due to both reduced stamen elongation and male and female fertilization defects. The hot5 null alleles show increased nitrate and nitroso species levels, and the heat sensitivity of both missense and null alleles is associated with increased NO species. Heat sensitivity is enhanced in wild-type and mutant plants by NO donors, and the heat sensitivity of hot5 mutants can be rescued by an NO scavenger. An NO-overproducing mutant is also defective in thermotolerance. Together, our results expand the importance of GSNOR-regulated NO homeostasis to abiotic stress and plant development.

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2008 Lee-Plant Cell Advance Online.pdf_eprint.pdf - Other
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Published date: March 2008
Organisations: Clinical & Experimental Sciences

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Local EPrints ID: 337824
URI: http://eprints.soton.ac.uk/id/eprint/337824
ISSN: 1040-4651
PURE UUID: ab529aab-bc20-4f55-899c-3c0f33ab84ad
ORCID for Martin Feelisch: ORCID iD orcid.org/0000-0003-2320-1158

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Date deposited: 04 May 2012 09:04
Last modified: 15 Mar 2024 03:41

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Contributors

Author: Ung Lee
Author: Chris Wie
Author: Bernadette O. Fernandez
Author: Martin Feelisch ORCID iD
Author: Elizabeth Vierling

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