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ERC

Triploid Block Report Summary

Project ID: 280496
Funded under: FP7-IDEAS-ERC
Country: Sweden

Final Report Summary - TRIPLOID BLOCK (Mechanisms of polyploidy-mediated postzygotic reproductive isolation)

Polyploidization is a widespread phenomenon among plants and is considered a major speciation mechanism. Before becoming evolutionary successful, newly formed polyploids often have to overcome fertility bottlenecks, because mating with partners of lower ploidy causes incompatibilities in the endosperm leading to the formation of mainly non-viable progeny. This reproductive barrier is called the triploid block. A main determinant for the failure of interploidy crosses is the endosperm, a nutritious tissue supporting embryo growth, similar to the functional role of the placenta in mammals. While it has been suggested that deregulated imprinted genes underpin dosage sensitivity of the endosperm, the molecular basis for this phenomenon remained unknown. In a genetic screen for suppressors of triploid seed abortion we have identified the paternally expressed imprinted gene ADMETOS (ADM) and could show that increased dosage of ADM causes triploid seed arrest. A large body of theoretical work predicted that deregulated imprinted genes establish the barrier to interploidy hybridization. Our study thus provides evidence strongly supporting this hypothesis and generates the molecular basis for our understanding of postzygotic hybridization barriers in plants.
We furthermore have collected evidence that paternal hypomethylation can bypass the interploidy hybridization barrier by alleviating the requirement of the epigenetic Polycomb Repressive Complex 2 (PRC2) in the endosperm. Bypass of the barrier is mediated by suppressed expression of imprinted genes like ADM. We show that the hypomethylated pollen genome causes de novo CHG methylation directed to FIS-PRC2 target genes, revealing that different epigenetic modifications can functionally substitute for each other. Our work presents a method and the underlying mechanism for the generation of viable triploids, providing an impressive example for the potential of epigenome manipulations for plant breeding.
Lastly, our work revealed that imprinted expression of paternally-expressed imprinted genes (PEGs) requires the FIS-PRC2 that directs the repressive modification H3 lysine 27 trimethylation (H3K27me3) to the maternal allele of PEGs. We could also show that PRC2-mediated H3K27me3 is preferentially localized to regions that are targeted by the DNA glycosylase DEMETER (DME), mechanistically linking DNA hypomethylation to imprinted gene expression. Our data furthermore suggest an absence of de novo DNA methylation in the early endosperm, providing an explanation how DME-mediated hypomethylation of the maternal genome is maintained after fertilization.

Contact

Eva Sundberg, (Head of Department)
Tel.: +46 18 67 3245
E-mail
Record Number: 193642 / Last updated on: 2017-01-13
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