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Plant Cell, Vol. 12, 2271-2282, November 2000, Copyright © 2000, American Society of Plant Physiologists

Hypomethylation Promotes Autonomous Endosperm Development and Rescues Postfertilization Lethality in fie Mutants

Rinke Vinkenooga, Melissa Spielmanb, Sally Adamsa, Robert L. Fischerc, Hugh G. Dickinsonb, and Rod J. Scotta
a Department of Biology and Biochemistry, University of Bath, Bath BA2 7AY, United Kingdom
b Department of Plant Sciences, University of Oxford, Oxford OX1 3RB, United Kingdom
c Department of Plant and Microbial Biology, University of California, Berkeley, California 94720-3102

Correspondence to: Rod J. Scott, bssrjs{at}bath.ac.uk (E-mail), 44-1225-826779 (fax)

In most flowering plants, fertilization is necessary for development of the central cell into endosperm, but in the fie-1 mutant of Arabidopsis, the central cell can proliferate autonomously. However, autonomous fie-1 endosperms do not develop completely: They have fewer nuclei than sexually produced endosperms, cellularization does not take place, and no clear distinction is seen between the different endosperm compartments. Here, we show that autonomous endosperm develop much further in hypomethylated than normally methylated fie-1 mutants, undergoing cellularization and regional specification to resemble endosperm in sexually produced wild-type seeds. Therefore, the combination of maternal hypomethylation and loss of FIE function enables formation of differentiated endosperm without fertilization. A maternal fie-1 mutation is also lethal to sexual seeds, even if the pollen donor is wild type. We report that sexual mutant fie-1 endosperms fail to cellularize and overproliferate, consistent with the hypothesis that embryo abortion may be due, at least in part, to a defect in endosperm development. Finally, we show that pollen from hypomethylated plants rescues fie-1 mutant seeds provided that it also donates a wild-type paternal FIE allele. These results are discussed in light of models for parent-of-origin effects on seed development.




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