Abstract
Interspecific hybridization often induces epigenetic remodeling that leads to transposon activation, gene expression changes, and loss of imprinting. These genomic changes can be deleterious and contribute to postzygotic hybrid incompatibility. In Arabidopsis, loss of genomic imprinting of PHERES1 and presumed failure of Polycomb Repressive Complex contributes to seed inviability observed in A. thaliana X A. arenosa interspecific hybrids. We used this species pair to further analyze the relationship between parentally biased gene expression and postzygotic hybrid incompatibility using two A. thaliana accessions, Col-0 and C24, with differential seed survival. We found that parentally biased expression was perturbed to a similar degree in both A. thaliana hybrids for PHERES1, HDG3, and six other normally paternally expressed genes. We propose that early genome remodeling and loss of imprinting of seed development genes induces lethality in both compatible and incompatible hybrids.
Highlights
Sexual reproduction in plants results in the formation of two zygotes, the embryo and the endosperm, which together with maternal tissue form the seed
We elected to map sequenced cDNA to the A. thaliana reference genes using an optimized C24 (S1 File, single nucleotide polymorphism (SNP) derived from C24 mRNA-seq libraries [31]) and A. arenosa (S2 File, SNPs derived from A. arenosa accessions Care and Strecno) SNP set to score allelic contribution (S1A Fig.)
Natural variation of parental regulation is mainly evident in the pollen parent We focused on candidate maternally expressed gene (MEG) and Perturbed in Arabidopsis Hybrids expressed gene (PEG) identified in control and hybrid crosses to determine how parental genotype affected their behavior
Summary
Sexual reproduction in plants results in the formation of two zygotes, the embryo and the endosperm, which together with maternal tissue form the seed. Methylated Regions (DMR) depending on parent of origin can be found in endosperm nuclear DNA, but not in embryo DNA, and are associated with genes that are preferentially expressed according to parent of origin. Another epigenetic pathway contributing to imprinting involves Polycomb Repressive Complex 2 (PRC2) and is exemplified by regulation of PHERES1 [8,9], a paternally
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