ArticlePlant physiology2006
Desensitization of GSTF8 induction by a prior chemical treatment is long lasting and operates in a tissue-dependent manner.
Article in Plant physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Molecular Insights into the Action Mechanism, Resistance Development, and Ecological Risks of Cyantraniliprole.International journal of molecular sciences · 2026Review
- Impact of pectin methylesterase on endophyte communities and pathogen resistance in Arabidopsis under heat stress.World journal of microbiology & biotechnology · 2026Article
- The ArabidopsisPlants (Basel, Switzerland) · 2019Article
- The Arabidopsis RNA Polymerase II Carboxyl Terminal Domain (CTD) Phosphatase-Like1 (CPL1) is a biotic stress susceptibility gene.Scientific reports · 2018Article
- A low-temperature-responsive element involved in the regulation of the Arabidopsis thaliana At1g71850/At1g71860 divergent gene pair.Plant cell reports · 2016Article
- Article
- Mitochondrial complex II has a key role in mitochondrial-derived reactive oxygen species influence on plant stress gene regulation and defense.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Mutant analysis in Arabidopsis provides insight into the molecular mode of action of the auxinic herbicide dicamba.PloS one · 2011Article
- Glutathione-indole-3-acetonitrile is required for camalexin biosynthesis in Arabidopsis thaliana.The Plant cell · 2011Article
- Glutathione transferases.The arabidopsis book · 2010Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Arabidopsis (Arabidopsis thaliana) GSTF8 gene is a member of the glutathione S-transferase (GST) family whose expression is induced by defense signals, certain chemical stresses, and some pathogens. Here, we have used transgenic plants and an in vivo imaging system to demonstrate that GSTF8 expression is subject to a distinct desensitization phenomenon because prior chemical treatment significantly reduces reactivation of the GSTF8 promoter by hydrogen peroxide, auxin, and salicylic acid. A GSTF8 null line had similar desensitization properties to wild type, demonstrating that GSTF8 protein levels are not responsible for desensitization. The resulting refractory period is unusually long lasting, with full recovery taking 4 d. Expression of the GSTF8 promoter following a second treatment occurred predominantly in newly formed tissue at the root tip, suggesting that desensitization is lost upon cell division. Expression of the endogenous GSTF8 gene and another GST gene, GSTF6, is also desensitized following treatment with hydrogen peroxide. The desensitization phenomenon can be activated by a very low concentration of inducer that is not sufficient to activate the GSTF8 promoter. These results demonstrate that activation of the GSTF8 promoter is not essential for eliciting desensitization. A key promoter sequence within the GSTF8 gene, the ocs element, is also affected by desensitization. Treatment with a phosphatase inhibitor prevents desensitization of GSTF8 expression and ocs element activity, suggesting that dephosphorylation of one or more proteins is required for desensitization to occur.
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