Hybrid incompatibility is generally viewed as a consequence of negative epistatic interactions between alleles that do not cause negative fitness effects in their parents. Substantial evidence in support of the model has accumulated over recent years. Nevertheless, there is evidence that hybrid incompatibility can have an epigenetic basis and results from deregulated small RNAs (sRNAs), causing changes in DNA methylation and transposable element (TE) activation. Epigenetically regulated loci can impact on the expression of nearby located genes. Alteration of dosage-sensitive gene expression builds hybridization barriers in the endosperm; however, it may also offer an explanation for transgressive effects in plant hybrids. In this review we highlight recent advances that illuminate the role of epigenetic pathways in establishing hybrid incompatibility in plants.
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