Why plants need more than one type of auxin

Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Plant science : an international journal of experimental plant biology. - 1985. - 180(2011), 3 vom: 03. März, Seite 454-60
1. Verfasser: Simon, Sibu (VerfasserIn)
Weitere Verfasser: Petrášek, Jan
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2011
Zugriff auf das übergeordnete Werk:Plant science : an international journal of experimental plant biology
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Review Indoleacetic Acids Indoles Phenylacetates Plant Growth Regulators Plant Proteins indolebutyric acid 061SKE27JP mehr... 4-chloroindole-3-acetic acid 2519-61-1 phenylacetic acid ER5I1W795A
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520 |a The versatile functionality and physiological importance of the phytohormone auxin is a major focus of attention in contemporary plant science. Recent studies have substantially contributed to our understanding of the molecular mechanisms underlying the physiological role of auxin in plant development. The mechanism of auxin action includes both fast responses not involving gene expression, possibly mediated by Auxin Binding Protein 1 (ABP1), and slower responses requiring auxin-regulated gene expression mediated by F-box proteins. These two mechanisms of action have been described to varying degrees for the major endogenous auxin indole-3-acetic acid (IAA) and for the synthetic auxins 2,4-dichlorophenoxyacetic acid (2,4-D) and naphthalene-1-acetic acid (NAA). However, in addition to IAA, plants synthesize three other compounds that are commonly regarded as "endogenous auxins", namely, 4-chloroindole-3-acetic acid (4-Cl-IAA), indole-3-butyric acid (IBA) and phenylacetic acid (PAA). Although a spectrum of auxinic effects has been identified for all these as well as several other endogenous compounds, we remain largely ignorant of many aspects of their mechanisms of action and the extent to which they contribute to auxin-regulated plant development. Here, we briefly summarize the action of IBA, 4-Cl-IAA and PAA, and discuss the extent to which their action overlaps with that of IAA or results from their metabolic conversions to IAA. Other possible pathways for their action are considered. We present a scheme for homeostatic regulation of IAA levels that embraces other endogenous auxins in terms of the described mechanism of auxin action including its receptor and downstream signal transduction events 
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