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Control of Fertilization-Independent Endosperm Development by the MEDEA Polycomb Gene in Arabidopsis

Tomohiro Kiyosue, Nir Ohad, Ramin Yadegari, Mike Hannon, Jose Dinneny, Derek Wells, Anat Katz, Linda Margossian, John J. Harada, Robert B. Goldberg and Robert L. Fischer
Proceedings of the National Academy of Sciences of the United States of America
Vol. 96, No. 7 (Mar. 30, 1999), pp. 4186-4191
Stable URL: http://www.jstor.org/stable/47786
Page Count: 6
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Control of Fertilization-Independent Endosperm Development by the MEDEA Polycomb Gene in Arabidopsis
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Abstract

Higher plant reproduction is unique because two cells are fertilized in the haploid female gametophyte. Egg and sperm nuclei fuse to form the embryo. A second sperm nucleus fuses with the central cell nucleus that replicates to generate the endosperm, a tissue that supports embryo development. To understand mechanisms that initiate reproduction, we isolated a mutation in Arabidopsis, f644, that allows for replication of the central cell and subsequent endosperm development without fertilization. When mutant f644 egg and central cells are fertilized by wild-type sperm, embryo development is inhibited, and endosperm is overproduced. By using a map-based strategy, we cloned and sequenced the F644 gene and showed that it encodes a SET-domain polycomb protein. Subsequently, we found that F644 is identical to MEDEA (MEA), a gene whose maternal-derived allele is required for embryogenesis [Grossniklaus, U., Vielle-Calzada, J.-P., Hoeppner, M. A. & Gagliano, W. B. (1998) Science 280, 446-450]. Together, these results reveal functions for plant polycomb proteins in the suppression of central cell proliferation and endosperm development. We discuss models to explain how polycomb proteins function to suppress endosperm and promote embryo development.

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