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First published online June 6, 2002; 10.1105/tpc.000869

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The Plant Cell, Vol. 14, 1391-1403, June 2002, Copyright © 2002,
American Society of Plant Biologists

The Homologous ABI5 and EEL Transcription Factors Function Antagonistically to Fine-Tune Gene Expression during Late Embryogenesis

Sandra Bensmihena, Sonia Rippa1,a, Guillaume Lamberta, Delphine Jublotb, Véronique Pautotb, Fabienne Granierc, Jérôme Giraudata and François Parcy2,a

a Institut des Sciences du Végétal, Centre National de la Recherche Scientifique, Avenue de la Terrasse, 91190 Gif-sur-Yvette, France
b Laboratoire de Biologie Cellulaire, Institut National de la Recherche Agronomique, Route de Saint Cyr, 78026 Versailles Cedex, France
c Station de Génétique et d'Amélioration des Plantes, Institut National de la Recherche Agronomique, Route de Saint-Cyr, 78026 Versailles Cedex, France

2 To whom correspondence should be addressed. E-mail francois.parcy{at}isv.cnrs-gif.fr; fax 33-1-69823695

In Arabidopsis, the basic leucine zipper transcription factor ABI5 activates several late embryogenesis–abundant genes, including AtEm1 and AtEm6. However, the expression of many other seed maturation genes is independent of ABI5. We investigated the possibility that ABI5 homologs also participate in the regulation of gene expression during seed maturation. We identified 13 ABI5-related genes in the Arabidopsis genomic sequence. RNA gel blot analysis showed that seven of these genes are active during seed maturation and that they display distinct expression kinetics. We isolated and characterized two mutant alleles of one of these genes, AtbZIP12/EEL. Unlike abi5, the eel mutations did not inhibit the expression of any of the maturation marker genes that we monitored. On the contrary, the accumulation of the AtEm1 and AtEm6 mRNAs was enhanced in eel mutant seeds compared with wild-type seeds. Gel mobility shift assays, combined with analysis of the genetic interactions among the eel and abi5 mutations, indicated that ABI5 and EEL compete for the same binding sites within the AtEm1 promoter. This study illustrates how two homologous transcription factors can play antagonistic roles to fine-tune gene expression.




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