This webinar discusses a project that sought to understand the parent-of-origin epigenetic mechanisms that regulate seed development in plants, with a particular emphasis on differentiating the maternal or paternal origin of epigenetics marks. Parental-specific epigenetic marks are established in the gametes and maintained after fertilization, resulting in parental epigenetic asymmetry. Epigenetic asymmetry causes parent-of-origin-specific gene expression, a phenomenon termed genomic imprinting. Imprinted genes play an important role in animal and plant development. In plants, genomic imprinting occurs in the seed, particularly in the endosperm, an ephemeral tissue that supports embryo growth similarly to the nourishing role of the mammalian placenta.
To study the mechanisms that maintain epigenetic asymmetry, Jordi Moreno-Romero and his colleagues at the Department of Plant Biology at the Uppsala BioCenter generated endosperm-specific genome-wide profiles of histone modifications (using chromatin immunoprecipitation followed by high throughput sequencing, ChIP-seq) and DNA methylation (using bisulfite-seq) at an early stage of seed development. By crossing two Arabidopsis accessions that differ in large numbers of sequence polymorphisms the researchers were able to differentiate the maternal or paternal origin of epigenetics marks.
During this webinar, Dr. Moreno-Romero discusses the findings of the study, which found that Polycomb-mediated H3 lysine 27 trimethylation (H3K27me3) is localized to DNA hypomethylated regions, linking DNA demethylation and H3K27me3 to imprinted gene expression.