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RESEARCH PAPER
1 Institute of Plant Biology & Zürich-Basel Plant Science Center, University of Zürich, CH-8008 Zürich, Switzerland , 2 Institute of Plant Sciences, Swiss Federal Institute of Technology (ETH), ETH Zentrum, LFW E47, CH-8092 Zürich, Switzerland
The Polycomb-group (PcG) proteins MEDEA, FERTILIZATION INDEPENDENT ENDOSPERM, and FERTILIZATION INDEPENDENT SEED2 regulate seed development in Arabidopsis by controlling embryo and endosperm proliferation. All three of these FIS-class proteins are likely subunits of a multiprotein PcG complex, which epigenetically regulates downstream target genes that were previously unknown. Here we show that the MADS-box gene PHERES1 (PHE1) is commonly deregulated in the fis-class mutants. PHE1 belongs to the evolutionarily ancient type I class of MADS-box proteins that have not yet been assigned any function in plants. Both MEDEA and FIE directly associate with the promoter region of PHE1, suggesting that PHE1 expression is epigenetically regulated by PcG proteins. PHE1 is expressed transiently after fertilization in both the embryo and the endosperm; however, it remains up-regulated in the fis mutants, consistent with the proposed function of the FIS genes as transcriptional repressors. Reduced expression levels of PHE1 in medea mutant seeds can suppress medea seed abortion, indicating a key role of PHE1 repression in seed development. PHE1 expression in a hypomethylated medea mutant background resembles the wild-type expression pattern and is associated with rescue of the medea seed-abortion phenotype. In summary, our results demonstrate that seed abortion in the medea mutant is largely mediated by deregulated expression of the type I MADS-box gene PHE1.
[Keywords: Arabidopsis; Polycomb group; MEDEA; MADS-box; embryo; endosperm]
Received December 11, 2002; revised version accepted April 29, 2003.
4 E-MAIL ckoehler{at}botinst.unizh.ch; FAX 41-01-634-82-04.
3 Present address: Department of Plant Systems Biology, Gent University, Ledeganckstraat 35, B-9000 Gent, Belgium
Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.257403.
Supplemental material is available at http://www.genesdev.org.
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