2016
DOI: 10.1073/pnas.1604458113
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Dynamic regulation of auxin oxidase and conjugating enzymes AtDAO1 and GH3 modulates auxin homeostasis

Abstract: The hormone auxin is a key regulator of plant growth and development, and great progress has been made understanding auxin transport and signaling. Here, we show that auxin metabolism and homeostasis are also regulated in a complex manner. The principal auxin degradation pathways in Arabidopsis include oxidation by Arabidopsis thaliana gene DIOXYGENASE FOR AUXIN OXIDATION 1/2 (AtDAO1/2) and conjugation by Gretchen Hagen3s (GH3s). Metabolic profiling of dao1-1 root tissues revealed a 50% decrease in the oxidati… Show more

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Cited by 121 publications
(126 citation statements)
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“…In fact, the latter possibility is supported by the observation that the IAA conjugates, IAA-Glu and IAA-Asp, the products of another major route of IAA inactivation, accumulate to much higher levels in the dao1 knockout mutant than in wild-type plants (5-7), whereas a gain-of-function allele of dao1 shows reduced levels of these conjugates (6). Consistent with this observation, an increase in the transcript level of GH3.3, one of the key enzymes in the conjugation of IAA to amino acids, in the dao1 loss-of-function mutant could be observed (5)(6)(7). This idea of the functional redundancy between the DAO-and the GH3-mediated auxin inactivation pathways was further supported by metabolite feeding experiments in which labeled auxin precursors were much more rapidly incorporated into the IAA conjugates, IAA-Asp and IAA-Glu, in the dao1 knockout mutant than in the wild-type controls (6).…”
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confidence: 58%
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“…In fact, the latter possibility is supported by the observation that the IAA conjugates, IAA-Glu and IAA-Asp, the products of another major route of IAA inactivation, accumulate to much higher levels in the dao1 knockout mutant than in wild-type plants (5-7), whereas a gain-of-function allele of dao1 shows reduced levels of these conjugates (6). Consistent with this observation, an increase in the transcript level of GH3.3, one of the key enzymes in the conjugation of IAA to amino acids, in the dao1 loss-of-function mutant could be observed (5)(6)(7). This idea of the functional redundancy between the DAO-and the GH3-mediated auxin inactivation pathways was further supported by metabolite feeding experiments in which labeled auxin precursors were much more rapidly incorporated into the IAA conjugates, IAA-Asp and IAA-Glu, in the dao1 knockout mutant than in the wild-type controls (6).…”
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confidence: 58%
“…Another possible mechanism that could be behind the large increase in IAA-Asp and IAA-Glu in the dao1 knockout, which was not originally considered, is an increase in the rates of IAA biosynthesis. In fact, when even a minor increase in auxin production was introduced, the mathematical model now predicted large increases in IAA conjugates, resulting in a much better match between the experimentally observed and model-predicted levels of IAA catabolites (7). Consistent with the increase in IAA biosynthesis needed for the mathematical model to accurately reflect the observed changes in auxin catabolites, an increase in the IAA precursor indole-3-pyruvic acid (IPyA) was detected in the dao1 loss-of-function mutant (6,7).…”
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confidence: 93%
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