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First published online February 20, 2008; 10.1104/pp.108.117044 Plant Physiology 146:1759-1772 (2008) © 2008 American Society of Plant Biologists OPEN ACCESS ARTICLE
Control of Compound Leaf Development by FLORICAULA/LEAFY Ortholog SINGLE LEAFLET1 in Medicago truncatula1,[C],[W],[OA]Plant Biology Division, The Samuel Roberts Noble Foundation, Ardmore, Oklahoma 73401 (H.W., J.C., J.W., M.T., G.L.,Y.L., K.S.M., R.C.); and Institut des Sciences du Vegetale, CNRS, 91198 Gif sur Yvette, France (P.R.)
Molecular genetic studies suggest that FLORICAULA (FLO)/LEAFY (LFY) orthologs function to control compound leaf development in some legume species. However, loss-of-function mutations in the FLO/LFY orthologs result in reduction of leaf complexity to different degrees in Pisum sativum and Lotus japonicus. To further understand the role of FLO/LFY orthologs in compound leaf development in legumes, we studied compound leaf developmental processes and characterized a leaf development mutant, single leaflet1 (sgl1), from the model legume Medicago truncatula. The sgl1 mutants exhibited strong defects in compound leaf development; all adult leaves in sgl1 mutants are simple due to failure in initiating lateral leaflet primordia. In addition, the sgl1 mutants are also defective in floral development, producing inflorescence-like structures. Molecular cloning of SGL1 revealed that it encodes the M. truncatula FLO/LFY ortholog. When properly expressed, LFY rescued both floral and compound leaf defects of sgl1 mutants, indicating that LFY can functionally substitute SGL1 in compound leaf and floral organ development in M. truncatula. We show that SGL1 and LFY differed in their promoter activities. Although the SGL1 genomic sequence completely rescued floral defects of lfy mutants, it failed to alter the simple leaf structure of the Arabidopsis thaliana plants. Collectively, our data strongly suggest that initiation of lateral leaflet primordia required for compound leaf development involves regulatory processes mediated by the SGL1 function in M. truncatula.
1 This work was supported by The Samuel Roberts Noble Foundation and by the European Union (EU FP6–GLIP project). 2 These authors contributed equally to the article. 3 Present address: Department of Microbiology and Molecular Genetics, Oklahoma State University, 307 Life Science East, Stillwater, OK 74078. 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: Rujin Chen (rchen{at}noble.org). [C] Some figures in this article are displayed in color online but in black and white in the print edition. [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.108.117044 * Corresponding author; e-mail rchen{at}noble.org. Received January 28, 2008; accepted February 14, 2008; published February 20, 2008. This article has been cited by other articles:
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