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PMID:17919906

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Citation

Wang, D, Pajerowska-Mukhtar, K, Culler, AH and Dong, X (2007) Salicylic acid inhibits pathogen growth in plants through repression of the auxin signaling pathway. Curr. Biol. 17:1784-90

Abstract

The phytohormone auxin regulates almost every aspect of plant development. At the molecular level, auxin induces gene expression through direct physical interaction with the TIR1-like F box proteins, which in turn remove the Aux/IAA family of transcriptional repressors [1-4]. A growing body of evidence indicates that many plant pathogens can either produce auxin themselves or manipulate host auxin biosynthesis to interfere with the host's normal developmental processes [5-11]. In response, plants probably evolved mechanisms to repress auxin signaling during infection as a defense strategy. Plants overaccumulating the defense signal molecule salicylic acid (SA) frequently display morphological phenotypes that are reminiscent of auxin-deficient or auxin-insensitive mutants, indicating that SA might interfere with auxin responses. By using the Affymetrix ATH1 GeneChip for Arabidopsis thaliana, we performed a comprehensive study of the effects of SA on auxin signaling [12]. We found that SA causes global repression of auxin-related genes, including the TIR1 receptor gene, resulting in stabilization of the Aux/IAA repressor proteins and inhibition of auxin responses. We demonstrate that this inhibitory effect on auxin signaling is a part of the SA-mediated disease-resistance mechanism.

Links

PubMed Online version:10.1016/j.cub.2007.09.025

Keywords

Arabidopsis/drug effects; Arabidopsis/genetics; Arabidopsis/physiology; Gene Expression Profiling; Genes, Plant/drug effects; Indoleacetic Acids/metabolism; Mutation; Oligonucleotide Array Sequence Analysis; Plant Diseases/genetics; Plant Growth Regulators/physiology; Plants, Genetically Modified; Salicylic Acid/metabolism; Salicylic Acid/pharmacology; Signal Transduction/drug effects; Thiadiazoles/pharmacology

Significance

Annotations

Gene product Qualifier GO ID GO term name Evidence Code with/from Aspect Notes Status


See also

References

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