Plant Cell Journal of Pharmacology and Experimental Therapeutics
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Plant Cell Advance Online Publication
Published on July 29, 2005; 10.1105/tpc.105.034637

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Received May 27, 2005
Returned for revision May 27, 2005
Accepted June 25, 2005

Maintenance of Embryonic Auxin Distribution for Apical-Basal Patterning by PIN-FORMED-Dependent Auxin Transport in Arabidopsis

Dolf Weijers 1, Michael Sauer 2, Olivier Meurette 3, Jirí Friml 2, Karin Ljung 4, Göran Sandberg 4, Paul Hooykaas 3, and Remko Offringa 3*

1 Developmental Genetics, Institute of Biology, Leiden University, Clusius Laboratory, 2333 AL Leiden, The Netherlands; Developmental Genetics, Center for Molecular Biology of Plants, University of Tübingen, D-72076 Tübingen, Germany
2 Developmental Genetics, Center for Molecular Biology of Plants, University of Tübingen, D-72076 Tübingen, Germany
3 Developmental Genetics, Institute of Biology, Leiden University, Clusius Laboratory, 2333 AL Leiden, The Netherlands
4 Umeå Plant Science Center, Department of Forest and Plant Physiology, Swedish University of Agricultural Sciences, SE 901 83 Umeå, Sweden

* To whom correspondence should be addressed. E-mail: offringa{at}rulbim.leidenuniv.nl.

Molecular mechanisms of pattern formation in the plant embryo are not well understood. Recent molecular and cellular studies, in conjunction with earlier microsurgical, physiological, and genetic work, are now starting to define the outlines of a model where gradients of the signaling molecule auxin play a central role in embryo patterning. It is relatively clear how these gradients are established and interpreted, but how they are maintained is still unresolved. Here, we have studied the contributions of auxin biosynthesis, conjugation, and transport pathways to the maintenance of embryonic auxin gradients. Auxin homeostasis in the embryo was manipulated by region-specific conditional expression of indoleacetic acid-tryptophan monooxygenase or indoleacetic acid-lysine synthetase, bacterial enzymes for auxin biosynthesis or conjugation. Neither manipulation of auxin biosynthesis nor of auxin conjugation interfered with auxin gradients and patterning in the embryo. This result suggests a compensatory mechanism for buffering auxin gradients in the embryo. Chemical and genetic inhibition revealed that auxin transport activity, in particular that of the PIN-FORMED1 (PIN1) and PIN4 proteins, is a major factor in the maintenance of these gradients.




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