Mechanisms for gene expression changes in polyploids. Allotetraploid formation is usually impaired by the hybridization barrier (red stop sign) between species. An allotetraploid may undergo rapid changes via genetic and epigenetic mechanisms, dosage regulation, and regulatory interactions. First, genetic changes (e.g., chromosomal rearrangements and gene loss) may cause gene expression and phenotypic variation []. Some duplicate genes may diverge expression patterns [] and the half-life of an active duplicate gene that becomes mutated or lost is estimated to be 2-7 million years []. Second, regulatory proteins produced from orthologous genes may generate incompatible products (heterodimers between red squares and blue circles), leading to silencing of one homoeologous gene. Alternatively, homoeologous proteins may perform better than the homozygous forms, which may explain overdominant effects on hybrid vigor []. Third, gene expression patterns may be reprogrammed by epigenetic changes in new allopolyploids. Hybridization or allopolyploidy induces formation of heterochromatin and euchromatin, resulting in gene silencing or activation via transcriptional and posttranscriptional mechanisms. Finally, dosage regulation suggests additive effects of gene expression in polyploids, leading to increased levels of expression and phenotypic variation. The dosage may augment the effects of hybridity (or genome merger) on gene expression and phenotypes. It is notable that these mechanisms are not mutually exclusive []. Gene expression changes may be selected by natural and/or artificial forces that facilitate adaptation and development.