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PMID:10205894

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Citation

Foster, R and Chua, NH (1999) An Arabidopsis mutant with deregulated ABA gene expression: implications for negative regulator function. Plant J. 17:363-72

Abstract

The physiological acclimation of plants to osmotic stresses involves a complex programme of gene regulation. In one signalling pathway, elevated levels of abscisic acid (ABA) activate a subset of stress genes. Because ABA responses lack a definable morphological phenotype, we have screened for mutants that exhibit deregulated ABA-responsive gene expression. To monitor this ABA response, a line of Arabidopsis thaliana carrying a transgene composed of the ABA-responsive Arabidopsis kin2 promoter fused to the coding sequence for the firefly luciferase gene, kin2::luc, was generated. Patterns of ABA-responsive luciferase activity were monitored by photon counting. In contrast to wild-type plants which display a transient activation of kin2::luc, an ABA deregulated gene expression mutant (ade1) exhibits both sustained and enhanced levels of transgene activity. Levels of kin2, cor47 and rab18 expression in ade1 plants are also enhanced and prolonged indicating that the molecular mechanism(s) altered in ade1 plants affects the regulation of other ABA-responsive genes. The mutant phenotype is specific for the ABA response as cold-inducible kin2 expression is unaltered in ade1 plants. Genetic analyses indicate that the ade1 mutant is a monogenic recessive trait. A role for negative regulator function in ABA signalling is discussed.

Links

PubMed

Keywords

Abscisic Acid/genetics; Arabidopsis/genetics; Arabidopsis Proteins; Base Sequence; DNA Primers; Gene Expression Regulation, Plant; Genes, Reporter; Luciferases/genetics; Plant Proteins/genetics

Significance

Annotations

Gene product Qualifier GO Term Evidence Code with/from Aspect Extension Notes Status

ARATH:COR47

acts_upstream_of_or_within

GO:0009737: response to abscisic acid

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete


See also

References

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