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Development. 2009 May;136(9):1509-17. doi: 10.1242/dev.025932.

A gain-of-function mutation in IAA18 alters Arabidopsis embryonic apical patterning.

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Department of Biology, University of North Carolina, Chapel Hill, NC 27599, USA.


Lateral organ emergence in plant embryos and meristems depends on spatially coordinated auxin transport and auxin response. Here, we report the gain-of-function iaa18-1 mutation in Arabidopsis, which stabilizes the Aux/IAA protein IAA18 and causes aberrant cotyledon placement in embryos. IAA18 was expressed in the apical domain of globular stage embryos, and in the shoot apical meristem and adaxial domain of cotyledons of heart stage embryos. Mutant globular embryos had asymmetric PIN1:GFP expression in the apical domain, indicating that IAA18-1 disrupts auxin transport. Genetic interactions among iaa18-1, loss-of-function mutations in ARF (Auxin response factor) genes and ARF-overexpressing constructs suggest that IAA18-1 inhibits activity of MP/ARF5 and other ARF proteins in the apical domain. The iaa18-1 mutation also increased the frequency of rootless seedlings in mutant backgrounds in which auxin regulation of basal pole development was affected. These results indicate that apical patterning requires Aux/IAA protein turnover, and that apical domain auxin response also influences root formation.

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