ArticleCommunications biology2026
Restoration of ancestral transcriptional plasticity contributes to plastic heterosis in fatty liver of hybrid ducks.
Article in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Restoration of ancestral transcriptional plasticity contributes to plastic heterosis in fatty liver of hybrid ducks.Communications biology · 2026Article
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4 authors.
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Abstract
Phenotypic plasticity enables organisms to modify their phenotypes in response to environmental fluctuations. Interspecific hybrids can inherit parental phenotypic plasticity and even exhibit enhanced physiological performance under analogous environmental shifts, a phenomenon termed as plastic heterosis. However, the genetic mechanisms underlying plastic heterosis remain poorly understood. Here, we explore the transcriptional profiling of overfeeding-induced fatty liver in Peking ducks (Anas platyrhynchos), Muscovy ducks (Cairina moschata), and their reciprocal hybrids. We find that genes associated with fatty acid catabolism retained their ancestral plasticity in Muscovy ducks but lost it in Peking ducks. The parental transcriptional plasticity is reshuffled in hybrid ducks during hybridization. Specifically, the expression pattern of 129 Peking-derived alleles is converted to those of Muscovy-derived alleles in both reciprocal hybrid ducks in response to overfeeding. Among these, eight fatty acid catabolism-related alleles that had lost plasticity in Peking ducks restore ancestral plasticity in hybrids. Our findings systematically characterize transcriptional changes linked to parental phenotypic plasticity and illuminate its evolutionary trajectory. In particular, the restoration of ancestral plasticity in interspecific hybrids may represent a mechanism contributing to plastic heterosis.
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