Plant Physiology Preview
Published on March 16, 2007; 10.1104/pp.107.096628
OPEN ACCESS ARTICLE
Received January 26, 2007
Accepted March 13, 2007
Specificity and Similarity of Functions of the Aux/IAA Genes in Auxin Signaling of Arabidopsis Revealed by Promoter-Exchange Experiments between MSG2/IAA19, AXR2/IAA3 and SLR/IAA14
Hideki Muto *, Masaaki K. Watahiki , Daisuke Nakamoto , Masataka Kinjo , and Kotaro T. Yamamoto
Department of Biological Sciences, Faculty of Science, Hokkaido University, Sapporo, 060-0810 Japan; Division of Biological Sciences, Graduate School of Science, Hokkaido University, Sapporo, 060-0810 Japan; Laboratory of Supramolecular Biophysics, Research Institute for Electronic Science, Hokkaido University, Sapporo, 060-0812 Japan
* Corresponding author; email: hidemuto{at}sci.hokudai.ac.jp.
As indicated by various and some overlapped phenotypes of the dominant mutants, the Aux/IAA genes of Arabidopsis thaliana concomitantly exhibit a functional similarity and differentiation. In order to evaluate the contributions of their expression patterns determined by promoter activity and molecular properties of their gene products to Aux/IAA function, we examined phenotypes of transgenic plants expressing the green fluorescent protein (GFP)-tagged msg2-1/iaa19, axr2-1/iaa7 or slr-1/iaa14 cDNA by the MSG2 or AXR2 promoter. When driven by the MSG2 promoter (pMSG2), each GFP-tagged cDNA caused the msg2-1 phenotype, that is, the wild-type stature in the mature-plant stage, long and straight hypocotyls in the dark, reduced lateral root formation, relatively mild agravitropic traits in hypocotyls, and a normal gravitropic response in roots. However, development of one or two cotyledonary primordia was often arrested in embryogenesis of the pMSG2::axr2-1::GFP and pMSG2::slr-1::GFP plants, resulting in monocotyledonary or no cotyledonary seedlings. Such defects in embryogenesis were never seen in pMSG2::msg2-1::GFP or the msg2-1, axr2-1 or slr-1 mutant. The MSG2 promoter-GUS staining showed that expression of MSG2 started specifically in cotyledonary primordia of the triangular-stage embryos. When driven by the AXR2 promoter (pAXR2), each GFP-tagged mutant cDNA caused, in principle, aberrant above-ground phenotypes of the corresponding dominant mutant. However, either the axr2-1::GFP or slr-1::GFP cDNA brought about dwarf, agravitropic stems almost identical to those of axr2-1, and the pAXR2::msg2-1::GFP and pAXR2::slr-1::GFP hypocotyls exhibited complete loss of gravitropism as did axr2-1. These results showed functional differences between the msg2-1, axr2-1 and slr-1 proteins, though some phenotypes were determined by the promoter activity.
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