Polycomb group complexes self-regulate imprinting of the Polycomb group gene MEDEA in Arabidopsis

PE Jullien, A Katz, M Oliva, N Ohad, F Berger - Current Biology, 2006 - cell.com
PE Jullien, A Katz, M Oliva, N Ohad, F Berger
Current Biology, 2006cell.com
Fertilization in flowering plants initiates the development of the embryo and endosperm,
which nurtures the embryo. A few genes subjected to imprinting are expressed in
endosperm from their maternal allele, while their paternal allele remains silenced [1–3].
Imprinting of the FWA gene involves DNA methylation [4]. Mechanisms controlling imprinting
of the Polycomb group (Pc-G) gene MEDEA (MEA)[5] are not yet fully understood [6–10].
Here we report that MEA imprinting is regulated by histone methylation. This epigenetic …
Summary
Fertilization in flowering plants initiates the development of the embryo and endosperm, which nurtures the embryo. A few genes subjected to imprinting are expressed in endosperm from their maternal allele, while their paternal allele remains silenced [1–3]. Imprinting of the FWA gene involves DNA methylation [4]. Mechanisms controlling imprinting of the Polycomb group (Pc-G) gene MEDEA (MEA) [5] are not yet fully understood [6–10]. Here we report that MEA imprinting is regulated by histone methylation. This epigenetic chromatin modification is mediated by several Pc-G activities during the entire plant life cycle. We show that Pc-G complexes maintain MEA transcription silenced throughout vegetative life and male gametogenesis. In endosperm, the maternal allele of MEA encodes an essential component of a Pc-G complex, which maintains silencing of the paternal MEA allele. Hence, we conclude that a feedback loop controls MEA imprinting. This feedback loop ensures a complete maternal control of MEA expression from both parental alleles and might have provided a template for evolution of imprinting in plants.
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