Frontier Leaders: Maternal pathways controlling plant embryogenesis
Ueli Grossniklaus - Universität Zürich
When |
12 Apr, 2011
from
11:00 am to 12:00 pm |
---|---|
Where | Auditorium |
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Frontier Leaders Seminar
Title: Maternal pathways controlling plant embryogenesis
Speaker: Ueli Grossniklaus
Affiliation: Universität Zürich
Abstract:
In flowering plants, seed development is initiated by double fertilization, where two pairs of gametes fuse to form the embryo and endosperm, respectively. Over the last decade, it has become apparent that epigenetic processes play a crucial role in seed development. However, it is not clear to what extent maternal contributions are involved in early embryogenesis. Defining the contributions and interactions of paternal and maternal genomes during embryo development is critical to understand the fundamental processes involved in heterosis, hybrid sterility, and reproductive isolation. We have used the model plant Arabidopsis thaliana to determine the parental contributions and their regulation during early embryogenesis. To this aim we combined deep-sequencing-based, allele-specific RNA profiling and genetic analyses. At the 2-4 cell stage there is a strong, genome-wide dominance of maternal transcripts, although transcripts are contributed by both parental genomes. At the globular stage the relative paternal contribution is higher, largely due to a gradual activation of the paternal genome. We identified two antagonistic maternal pathways that control these parental contributions. Paternal alleles are initially downregulated by the chromatin siRNA pathway, linked to DNA and histone methylation, while transcriptional activation requires the maternal activity of the histone chaperone complex CAF1. We propose that the interplay between activating and repressing maternal factors defines the distinct timing and kinetics of paternal genome activation for each locus. In summary, our results define novel maternal epigenetic pathways controlling the parental contributions in plant embryos, which are distinct from those regulating genomic imprinting.