Abstract
The major auxin, indole-3-acetic acid (IAA), is associated with a plethora of growth and developmental processes including embryo development, expansion growth, cambial activity, and the induction of lateral root growth. Accumulation of the auxin precursor indole-3-acetamide (IAM) induces stress related processes by stimulating abscisic acid (ABA) biosynthesis. How IAM signaling is controlled is, at present, unclear. Here, we characterize the ami1 rooty double mutant, that we initially generated to study the metabolic and phenotypic consequences of a simultaneous genetic blockade of the indole glucosinolate and IAM pathways in Arabidopsis thaliana. Our mass spectrometric analyses of the mutant revealed that the combination of the two mutations is not sufficient to fully prevent the conversion of IAM to IAA. The detected strong accumulation of IAM was, however, recognized to substantially impair seed development. We further show by genome-wide expression studies that the double mutant is broadly affected in its translational capacity, and that a small number of plant growth regulating transcriptional circuits are repressed by the high IAM content in the seed. In accordance with the previously described growth reduction in response to elevated IAM levels, our data support the hypothesis that IAM is a growth repressing counterpart to IAA.
Highlights
IntroductionThe auxin indole-3-acetic acid (IAA) is a major endogenous growth factor in plants and is linked with a great variety of different developmental processes and adaptive responses, including elongation growth, polar development, cambial activity, gravitropism and phototropism, respectively
indole-3-acetic acid (IAA) levels, downstream mutations in sur1 translate into significantly increased IAOx, IAM, and IAA contents, suggesting the channeling of IAOx into IAA to proceed via IAM
The significantly elevated IAA levels in those mutants provoke strong auxin overproduction-related phenotypes, including epinasty of cotyledons and true leaves, significant amplification of lateral root numbers, and an increased root hair number and density [21,23]. Picking up on these lines of evidence, which suggest a purely auxin-mediated phenotype, we reasoned that a genetic block of the IAM pathway (IAOx→IAM→IAA) in indole glucosinolate mutants may restore a wild type phenotype, due to the impaired conversion of IAM to IAA
Summary
The auxin indole-3-acetic acid (IAA) is a major endogenous growth factor in plants and is linked with a great variety of different developmental processes and adaptive responses, including elongation growth, polar development, cambial activity, gravitropism and phototropism, respectively. It is not surprising that IAA is recognized as an essential phytohormone necessary to ensure optimal plant growth and development [1,2]. The main source of auxin in plants is the indole-3-pyruvate (IPyA) pathway, encompassing tryptophan aminotransferases (TAA1/TAR2) and flavin containing monooxygenases (YUC1-11) that convert L-tryptophan (L-Trp) to IAA via the intermediate IPyA [3,4].
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