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First published online March 25, 2009; 10.1104/pp.109.137034

Plant Physiology 150:205-216 (2009)
© 2009 American Society of Plant Biologists

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DEVELOPMENT AND HORMONE ACTION

Studies of aberrant phyllotaxy1 Mutants of Maize Indicate Complex Interactions between Auxin and Cytokinin Signaling in the Shoot Apical Meristem1,[W],[OA]

Byeong-ha Lee2, Robyn Johnston2, Yan Yang, Andrea Gallavotti, Mikiko Kojima, Bruno A.N. Travençolo, Luciano da F. Costa, Hitoshi Sakakibara and David Jackson*

Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724 (B.-h.L., R.J., Y.Y., A.G., D.J.); Department of Life Science, Sogang University, Seoul 121–742, Korea (B.-h.L.); University of Amsterdam, Amsterdam, 1098SM, The Netherlands (Y.Y.); Section of Cell and Development Biology, University of California, San Diego, La Jolla, California 92093–0116 (A.G.); Plant Science Center, RIKEN, Tsurumi, Yokohama 230–0045, Japan (M.K., H.S.); and Instituto de Física de São Carlos, Universidade de São Paulo, São Carlos, São Paulo 13560–970, Brazil (B.A.N.T., L.d.F.C.)

One of the most fascinating aspects of plant morphology is the regular geometric arrangement of leaves and flowers, called phyllotaxy. The shoot apical meristem (SAM) determines these patterns, which vary depending on species and developmental stage. Auxin acts as an instructive signal in leaf initiation, and its transport has been implicated in phyllotaxy regulation in Arabidopsis (Arabidopsis thaliana). Altered phyllotactic patterns are observed in a maize (Zea mays) mutant, aberrant phyllotaxy1 (abph1, also known as abphyl1), and ABPH1 encodes a cytokinin-inducible type A response regulator, suggesting that cytokinin signals are also involved in the mechanism by which phyllotactic patterns are established. Therefore, we investigated the interaction between auxin and cytokinin signaling in phyllotaxy. Treatment of maize shoots with a polar auxin transport inhibitor, 1-naphthylphthalamic acid, strongly reduced ABPH1 expression, suggesting that auxin or its polar transport is required for ABPH1 expression. Immunolocalization of the PINFORMED1 (PIN1) polar auxin transporter revealed that PIN1 expression marks leaf primordia in maize, similarly to Arabidopsis. Interestingly, maize PIN1 expression at the incipient leaf primordium was greatly reduced in abph1 mutants. Consistently, auxin levels were reduced in abph1, and the maize PIN1 homolog was induced not only by auxin but also by cytokinin treatments. Our results indicate distinct roles for ABPH1 as a negative regulator of SAM size and a positive regulator of PIN1 expression. These studies highlight a complex interaction between auxin and cytokinin signaling in the specification of phyllotactic patterns and suggest an alternative model for the generation of altered phyllotactic patterns in abph1 mutants. We propose that reduced auxin levels and PIN1 expression in abph1 mutant SAMs delay leaf initiation, contributing to the enlarged SAM and altered phyllotaxy of these mutants.


1 This work was supported by the Conselho Nacional de Desenvolvimento Científico e Tecnológico (grant no. 308231/03–1 to L.d.F.C.), by the Fundação de Amparo à Pesquisa do Estado de São Paulo (grant no. 03/13072–8 to B.A.N.T.), by a Cold Spring Harbor Laboratory association fellowship to A.G., by a Special Research Grant of Sogang University to B.-h.L., and by the National Science Foundation (grant no. IOB 0642707 to B.-h.L., R.J., and D.J. and grant no. DBI–0501862 to Y.Y. and D.J.).

2 These authors contributed equally to the article.

The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: David Jackson (jacksond{at}cshl.edu).

[W] The online version of this article contains Web-only data.

[OA] Open Access articles can be viewed online without a subscription.

www.plantphysiol.org/cgi/doi/10.1104/pp.109.137034

* Corresponding author; e-mail jacksond{at}cshl.edu.

Received February 12, 2009; accepted March 19, 2009; published March 25, 2009.







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