Pauline E Jullien,1,2 Assaf Mosquna,3 Mathieu Ingouff,1 Tadashi Sakata,1 Nir Ohad,3 and Frédéric Berger1*, PLoS Biol. 2008 August; 6(8): e194.
1 Chromatin and Reproduction Group, Temasek Life Sciences Laboratory, National University of Singapore, Singapore, Republic of Singapore
2 Zentrum für Molekularbiologie der Pflanzen (ZMBP), Entwicklungsgenetik, Universität Tübingen, Tübingen, Germany
3 Department of Plant Sciences, Faculty of Life Sciences, Tel-Aviv University, Tel-Aviv, Israel
Abstract
Parental genomic imprinting causes preferential expression of one of the two parental alleles. In mammals, differential sex-dependent deposition of silencing DNA methylation marks during gametogenesis initiates a new cycle of imprinting. Parental genomic imprinting has been detected in plants and relies on DNA methylation by the methyltransferase MET1. However, in contrast to mammals, plant imprints are created by differential removal of silencing marks during gametogenesis. In Arabidopsis, DNA demethylation is mediated by the DNA glycosylase DEMETER (DME) causing activation of imprinted genes at the end of female gametogenesis. On the basis of genetic interactions, we show that in addition to DME, the plant homologs of the human Retinoblastoma (Rb) and its binding partner RbAp48 are required for the activation of the imprinted genes FIS2 and FWA. This Rb-dependent activation is mediated by direct transcriptional repression of MET1 during female gametogenesis. We have thus identified a new mechanism required for imprinting establishment, outlining a new role for the Retinoblastoma pathway, which may be conserved in mammals. | 
