Here is the title and abstract:
| Title | Disrupted imprinting, the large X-effect, and extreme hybrid overgrowth in hamsters | ||
| Abstract |
Extreme abnormal growth is a recurrent phenotype in mammalian hybrids, indicating that disruption of development may play an important role in mammalian speciation. Disrupted genomic imprinting - the parent-specific epigenetic silencing of one allele - resulting in dosage imbalances between growth factors and repressors has been hypothesized to be the predominant cause of abnormal hybrid growth in mammals. However, genetic imprinting may also expose hybrid incompatibilities through the hemizygous expression of genes. Here we combined genome-wide transcriptomic and quantitative genetic experiments to dissect the genetic underpinnings of extreme overgrowth that manifests in hybrids between two closely related species of dwarf hamsters. Specifically we tested for disrupted imprinting and differences in the expression of growth-related genes in overgrown hybrid placenta. We found that large hybrids show evidence for disrupted paternal imprinting and differential expression of imprinted genes in general. Surprisingly, the disruption of paternal imprinting is associated with reduced gene expression. As paternally imprinted genes tend to repress offspring growth, these data suggest that overgrowth is associated with a reduction in growth repressors rather than an excess of growth factors. Using QTL mapping, we have further identified the X chromosome as the predominant factor explaining hybrid placental overgrowth. However, expression and imprinting status of the X chromosome is not significantly disrupted, indicating that X-linked genetic incompatibilities are not caused by chromosome-wide misregulation. Collectively, our data underscore a central role for both disrupted epigenetic processes and the X chromosome in driving the evolution of abnormal hybrid growth in mammals.
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