Abstract
Auxin is a phytohormone involved in cell elongation and division. Levels of indole-3-acetic acid (IAA), the primary auxin, are tightly regulated through biosynthesis, degradation, sequestration, and transport. IAA is sequestered in reversible processes by adding amino acids, polyol or simple alcohols, or sugars, forming IAA conjugates, or through a two-carbon elongation forming indole-3-butyric acid. These sequestered forms of IAA alter hormone activity. To gain a better understanding of how auxin homeostasis is maintained, we have generated Arabidopsis (Arabidopsis thaliana) mutants that combine disruptions in the pathways, converting IAA conjugates and indole-3-butyric acid to free IAA. These mutants show phenotypes indicative of low auxin levels, including delayed germination, abnormal vein patterning, and decreased apical dominance. Root phenotypes include changes in root length, root branching, and root hair growth. IAA levels are reduced in the cotyledon tissue but not meristems or hypocotyls. In the combination mutants, auxin biosynthetic gene expression is increased, particularly in the YUCCA/Tryptophan Aminotransferase of Arabidopsis1 pathway, providing a feedback mechanism that allows the plant to compensate for changes in IAA input pathways and maintain cellular homeostasis.
Highlights
indole-3-acetic acid (IAA)-amino acid conjugates are formed by GH3 enzymes (Staswick et al, 2005)
The ill2 iar3 ibr3 and ill2 iar3 ilr1 ibr1 mutants showed resistance to root inhibition on IAA-Ala and indole-3butyric acid (IBA), as expected based on the parent mutant phenotypes. mes17 containing mutants were confirmed by expression analysis (Supplemental Figure 1, data not shown)
Specific transcriptional activation and repression pathways occur based on the level of free IAA in an individual cell, leading to physiological changes in plant growth and development
Summary
IAA-amino acid conjugates are formed by GH3 enzymes (Staswick et al, 2005) These genes were identified as auxin inducible and maintain auxin homeostasis at high IAA levels by conjugating, inactivating, IAA (Hagen and Guilfoyle, 1985; Staswick et al, 2005). An iamt1-D dominant mutant causes curled leaves and IAMT overexpression disrupts gravitropic responses and root elongation, mediated by changes in auxin-induced gene expression (Qin et al, 2005). Feeding experiments with labeled IBA showed loss of these enzymes directly disrupted IBA conversion to IAA (Zolman et al, 2008; Strader et al, 2011) Mutants in these four enzymes have defects in plant development, including lateral rooting, vasculature patterning, and root hair expansion, mediated by changes in auxin-induced gene expression (Zolman et al, 2000; Strader et al, 2011). To compensate for low auxin levels, the plant activates a specific set of auxin-biosynthetic genes, including those involved in de novo IAA biosynthesis
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