Control of fertilization-independent endosperm development by the MEDEA polycomb gene in Arabidopsis
Tomohiro Kiyosue,Nir Ohad,Ramin Yadegari,Mike Hannon,José R. Dinneny,Derek Wells,Anat Katz,Linda Margossian,John J. Harada,Robert B. Goldberg,Robert L. Fischer,Robert L. Fischer +11 more
TLDR
Grossniklaus et al. as mentioned in this paper used a map-based strategy to identify a mutation in Arabidopsis, f644, that allows for replication of the central cell and subsequent endosperm development without fertilization.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.read more
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Reference EntryDOI
Epigenetic Reprogramming in Mammalian Development
TL;DR: In this chapter, a summary is provided of the current knowledge of epigenetic reprogramming mechanisms, and with the role of DNA methylation in particular is discussed.
Journal ArticleDOI
DEMETER, a DNA Glycosylase Domain Protein, Is Required for Endosperm Gene Imprinting and Seed Viability in Arabidopsis
Yeonhee Choi,Mary Gehring,Lianna M. Johnson,Mike Hannon,John J. Harada,Robert B. Goldberg,Steven E. Jacobsen,Robert L. Fischer +7 more
TL;DR: The authors isolated mutations in Arabidopsis to understand how the female gametophyte controls embryo and endosperm development and identified the DEMETER (DME) gene, which is required for maternal allele expression of the imprinted MEDEA (MEA) Polycomb gene in the central cell andendosperm.
Journal ArticleDOI
Active DNA demethylation mediated by DNA glycosylases.
TL;DR: Evidence suggests that active DNA demethylation in mammalian cells is also mediated at least in part by a base excision repair pathway where the AID/Apobec family of deaminases convert 5-methylcytosine to thymine followed by G/T mismatch repair by the DNA glycosylase MBD4 or TDG.
Journal ArticleDOI
DEMETER DNA Glycosylase Establishes MEDEA Polycomb Gene Self-Imprinting by Allele-Specific Demethylation
Mary Gehring,Jin Hoe Huh,Tzung-Fu Hsieh,Jon Penterman,Yeonhee Choi,John J. Harada,Robert B. Goldberg,Robert L. Fischer +7 more
TL;DR: DME is responsible for endosperm maternal-allele-specific hypomethylation at the MEA gene, which establishes MEA imprinting by removing 5-methylcytosine to activate the maternal allele and is subsequently maintained in theendosperm by maternal MEA silencing the paternal allele.
Journal ArticleDOI
The role of RNA interference in heterochromatic silencing
TL;DR: Heterochromatin has emerged as a key factor in epigenetic regulation of gene expression, chromosome behaviour and evolution.
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