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Expression data in response to neonicotinoid insecticides
Mary C Wildermuth, University of California Berkeley, Department of Plant and Microbial Biology, Berkeley, California (mwildermuth@berkeley.edu)
Experiment design (8 hybridizations)
compound
•untreated •CLO •IMI •SA

This experiment has been imported by PLEXdb from NCBI GEO (GSE20188)

Series_summary:
Neonicotinoid insecticides control crop pests ba...[complete overview]

Experiment     Expression     Hybridizations & Samples     Quality Control     Compare Treatments     Downloads    

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Experiment Name: Expression data in response to neonicotinoid insecticides
Accession No: AT110
Microarray: ATH1-121501
Visibility: public
Experiment Type:
Experiment Factor(s):
compound
•untreated   •CLO   •IMI   •SA
Quality Control: biological replicates
Treatment summary:
 compound  # replicates
 untreated  2
 CLO  2
 IMI  2
 SA  2
Total hybridizations: 8
Description: This experiment has been imported by PLEXdb from NCBI GEO (GSE20188)

Series_summary:
Neonicotinoid insecticides control crop pests based on their action as agonists at the insect nicotinic acetylcholine receptor which accepts chloropyridinyl- and chlorothiazolyl- analogs almost equally well. In some cases, these compounds have also been reported to enhance plant vigor and (a)biotic stress tolerance, independent of their insecticidal function. However, this mode of action has not been specifically defined. Using Arabidopsis thaliana, we show that the neonicotinoid compounds, imidacloprid (IMI) and clothianidin (CLO), via their 6-chloropyridinyl-3-carboxylic acid and 2-chlorothiazolyl-5-carboxylic acid metabolites, respectively, induce salicylic acid (SA) – associated plant responses. SA is a phytohormone best known for its role in plant defense against pathogens and as an inducer of systemic acquired resistance; however, it can also modulate abiotic stress responses. These neonicotinoids effect a similar global transcriptional response to that of SA including genes involved in (a)biotic stress response. Furthermore, similar to SA, IMI and CLO induce systemic acquired resistance resulting in reduced growth of a powdery mildew pathogen. The action of CLO induces the endogenous synthesis of SA via the SA biosynthetic enzyme ICS1, with ICS1 required for CLO-induced accumulation of SA, expression of the SA marker PR1, and fully enhanced resistance to powdery mildew. In contrast, the action of IMI does not induce endogenous synthesis of SA. Instead, IMI is further bioactivated to 6-chloro-2-hydroxypyridinyl-3-carboxylic acid, which is shown here to be a potent inducer of PR1 and inhibitor of SA-sensitive enzymes. Thus, via different mechanisms, these chloropyridinyl- and chlorothiazolyl- neonicotinoids induce SA responses associated with enhanced stress tolerance.

Series_overall_design:
response to neonicotinoid insecticides
Publication: 'Neonicotinoid insecticides induce salicylate-associated plant defense responses.', Ford KA, Casida JE, Chandran D, Gulevich AG, Okrent RA, Durkin KA, Sarpong R, Bunnelle EM, Wildermuth MC.
Proc Natl Acad Sci U S A 2010 Oct 12;107(41):17527-32.
pubmed: 20876120
Created: 2012-01-19 09:12:16
Last Update: 2012-01-19 09:59:17
Released: 2012-01-19
GEO Accession GSE20188
Submitter: PLEXdb Curator
Name: Mary C Wildermuth
Institution: University of California Berkeley, Department of Plant and Microbial Biology, Berkeley, California
Head of Laboratory: Mary C Wildermuth
email(s):
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