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First published online January 19, 2005; 10.1105/tpc.104.026716

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The Plant Cell 17:464-474 (2005)
© 2005 American Society of Plant Biologists

The Branching Gene RAMOSUS1 Mediates Interactions among Two Novel Signals and Auxin in Pea

Eloise Fooa,1, Erika Bullierb, Magali Goussotb, Fabrice Foucherb,2, Catherine Rameaub and Christine Anne Beveridgea,3

a Australian Research Council Centre of Excellence for Integrative Legume Research, University of Queensland, St. Lucia, Queensland, 4072, Australia
b Station de Génétique et d'Amélioration des Plantes, Institut J.P. Bourgin, Institut National de la Recherche Agronomique, 78026, Versailles Cedex, France

3 To whom correspondence should be addressed. E-mail c.beveridge{at}botany.uq.edu.au; fax 61-0-7-3365-1699.

In Pisum sativum, the RAMOSUS genes RMS1, RMS2, and RMS5 regulate shoot branching via physiologically defined mobile signals. RMS1 is most likely a carotenoid cleavage enzyme and acts with RMS5 to control levels of an as yet unidentified mobile branching inhibitor required for auxin inhibition of branching. Our work provides molecular, genetic, and physiological evidence that RMS1 plays a central role in a shoot-to-root-to-shoot feedback system that regulates shoot branching in pea. Indole-3-acetic acid (IAA) positively regulates RMS1 transcript level, a potentially important mechanism for regulation of shoot branching by IAA. In addition, RMS1 transcript levels are dramatically elevated in rms3, rms4, and rms5 plants, which do not contain elevated IAA levels. This degree of upregulation of RMS1 expression cannot be achieved in wild-type plants by exogenous IAA application. Grafting studies indicate that an IAA-independent mobile feedback signal contributes to the elevated RMS1 transcript levels in rms4 plants. Therefore, the long-distance signaling network controlling branching in pea involves IAA, the RMS1 inhibitor, and an IAA-independent feedback signal. Consistent with physiological studies that predict an interaction between RMS2 and RMS1, rms2 mutations appear to disrupt this IAA-independent regulation of RMS1 expression.




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