Genomic imprinting, disrupted placental expression, and speciation

Area of Science:

• Evolutionary genetics
• Developmental biology
• Mammalian speciation

Background:

• Hybrid mammals often exhibit extreme parent-of-origin growth effects.
• These effects are hypothesized to stem from disrupted genetic imprinting (parent-specific epigenetic gene silencing) during development.
• The loss of imprinting (LOI) model suggests abnormal hybrid growth results from imbalanced gene dosage in placentas.

Purpose of the Study:

• To investigate the role of disrupted gene expression and imprinting in mammalian hybrid inviability.
• To test the hypothesis that abnormal hybrid growth is caused by loss of imprinting (LOI) in hybrid placentas.
• To analyze placental gene expression in reciprocal dwarf hamster hybrids exhibiting extreme parent-of-origin growth effects.

Main Methods:

• Analysis of placental gene expression in reciprocal dwarf hamster hybrids.
• Comparison of gene expression patterns in enlarged hybrid placentas versus parental species.
• Examination of transgressive expression and biallelic expression of growth-related genes.

Main Results:

• Massively enlarged hybrid placentas showed transgressive expression of growth-related genes.
• Extensive biallelic expression of paternally silenced genes was observed in hybrids.
• Widespread disruption of paternal silencing was paradoxically coupled with overall reduced gene expression levels.

Conclusions:

• Observed gene expression patterns contradict the predictions of the loss of imprinting (LOI) model.
• Hybrid misexpression of dosage-sensitive genes is likely driven by regulatory mechanisms other than LOI.
• Disrupted gene expression and imprinting play a role in mammalian hybrid inviability, but the generality of the LOI model is questioned.