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First published online April 29, 2002; 10.1105/tpc.001248

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The Plant Cell, Vol. 14, 1017-1031, May 2002, Copyright © 2002,
American Society of Plant Biologists

hydra Mutants of Arabidopsis Are Defective in Sterol Profiles and Auxin and Ethylene Signaling

Martin Souter1,a, Jennifer Topping1,a, Margaret Pullena, Jiri Frimlb, Klaus Palmeb, Rachel Hackettc, Don Griersonc and Keith Lindsey2,a

a Integrative Cell Biology Laboratory, School of Biological and Biomedical Sciences, University of Durham, South Road, Durham DH1 3LE, United Kingdom
b Max-Delbrück Laboratorium, Carl von Linne Weg 10, D-50829 Köln, Germany
c Plant Science Division, University of Nottingham, Sutton Bonington Campus, Loughborough LE12 5RD, United Kingdom

2 To whom correspondence should be addressed. E-mail keith.lindsey{at}durham.ac.uk; fax 44-191-374-2417

The hydra mutants of Arabidopsis are characterized by a pleiotropic phenotype that shows defective embryonic and seedling cell patterning, morphogenesis, and root growth. We demonstrate that the HYDRA1 gene encodes a {Delta}8-{Delta}7 sterol isomerase, whereas HYDRA2 encodes a sterol C14 reductase, previously identified as the FACKEL gene product. Seedlings mutant for each gene are similarly defective in the concentrations of the three major Arabidopsis sterols. Promoter::reporter gene analysis showed misexpression of the auxin-regulated DR5 and ACS1 promoters and of the epidermal cell file–specific GL2 promoter in the mutants. The mutants exhibit enhanced responses to auxin. The phenotypes can be rescued partially by inhibition of auxin and ethylene signaling but not by exogenous sterols or brassinosteroids. We propose a model in which correct sterol profiles are required for regulated auxin and ethylene signaling through effects on membrane function.




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