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Symposium III: Advances in plant reproductive biology

Abs # 30004: Arabidopsis RBR1 and MSI1 integrate cell cycle and epigentic regulation of female gametophyte and seed development

Presenter: Gruissem, Wilhelm , wilhelm.gruissem@ipw.biol.ethz.ch
AuthorsEbel, Chantal  (A)   Hennig, Lars  (A)   Köhler, Claudia  (B)   Mariconti, Luisa  (A)   Grossniklaus, Ueli  (B) (C)  Gruissem, Wilhelm  (A) (C) 
Affiliations: (A): Institute of Plant Sciences, Swiss Federal Institute of Technology, ETH Center, 8092 Zürich, Switzerland
(B): Institute of Plant Biology, University of Zurich, Zollikerstrasse 107, 8050 Zurich, Switzerland
(C): Zurich-Basel Plant Science Center
Web Site:http://www.pb.ethz.ch

Animals and plants have evolved complex regulatory mechanisms that direct development and cell differentiation, but the integration of these processes with the cell cycle are not well understood. Current models suggest that mammalian Rb, and perhaps the plant homolog RBR1, has a dual role in regulating cell cycle progression and cell differentiation. Rb family proteins are corepressors of the E2F/DP family of transcription factors, and together they control various aspects of cell cycle progression. Rb also functions to maintain the differentiation status of several cell types and to protect cells from apoptosis. Complete loss of Arabidopsis RBR1 or MSI1 function is gametophytically lethal. Nuclei in the region of the female egg apparatus continue to proliferate after megagametogenesis, indicating that RBR1 is required to arrest the nuclei of the egg apparatus prior to fertilization. The endosperm nucleus also proliferates in RBR1 or MSI1 loss-of-function mutants, thus establishing a functional link between these two proteins. MSI1 interacts with RBR1 and FIE, which is part of a complex with MEA, a protein similar to the Drosophila Polycomb group (PcG) protein E(Z). But in contrast to rbr1, the egg apparatus does not overproliferate in msi1 or other fertilization independent seed (fis) mutants, suggesting that nuclear proliferation is controlled by different mechanisms in the egg apparatus and endosperm. This work is supported by the Swiss National Science Foundation and the European Cell Cycle Consortium

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