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First published online 12 September 2007
doi: 10.1242/dev.009027
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1 Institute of Plant Sciences and Zürich-Base Plant Science Center, Swiss
Federal Institute of Technology, ETH Centre, CH-8092 Zürich,
Switzerland.
2 Institute of Biology II, University of Freiburg, Schänzlestr. 1, 79104
Freiburg, Germany.
* Author for correspondence (e-mail: koehlerc{at}ethz.ch)
Accepted 2 August 2007
Polycomb group (PcG) proteins are evolutionary conserved proteins that stably maintain established transcriptional patterns over cell generations. The FERTILIZATION INDEPENDENT SEED (FIS) PcG complex from plants has a similar composition to the Polycomb repressive complex 2 from animals. Mutations in FIS genes cause parent-of-origin-dependent seed abortion. Every seed inheriting a mutant fis allele from the mother is destined to abort, regardless of the presence of a wild-type paternal allele. We tested in Arabidopsis whether the parent-of-origin-dependent seed abortion caused by lack of the FIS subunit MSI1 is caused by parental imprinting of the MSI1 gene. Our data show that MSI1 is not an imprinted gene and that early paternal MSI1 expression is not sufficient to rescue msi1 mutant seeds. By contrast, expression of MSI1 in msi1 female gametophytes is necessary to restore normal seed development, strongly arguing that the female gametophytic effect of fis mutants is caused by a functional requirement for an intact FIS complex in the female gametophyte. Thus, FIS-mediated expression patterns established in the female gametophyte can impact on seed development, establishing fis mutants as true female gametophytic maternal-effect mutants.
Key words: Arabidopsis, Epigenetics, FERTILIZATION INDEPENDENT SEED genes, Imprinting, Polycomb group proteins
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