Dejeux Léo, Saclier Nathanaëlle, Tariel-Adam Juliette, Hoareau Maxime, Lefébure Tristan, Konecny Lara, Plénet Sandrine, Luquet Emilien
Université Claude Bernard Lyon 1, LEHNA UMR 5023, CNRS, ENTPE, Villeurbanne, France.
ISEM, Univ Montpellier, CNRS, IRD, Montpellier, France.
Heredity (Edinb). 2025 Jun 13. doi: 10.1038/s41437-025-00775-9.
Inducible defences in response to predation risk are a well-known example of adaptive phenotypic plasticity. Although inducible defences have been studied mainly within a generation (within-generational plasticity), there is now clear evidence that ancestral exposure to predation risk can influence the defences expressed by offspring, even if they have not been exposed themselves (transgenerational plasticity). The molecular mechanisms allowing the transmission of environmental information across generations are not well understood. In this study, we combined measures of antipredator responses (behavioural and morphological) with transcriptomic investigations across two generations in the freshwater snail Physa acuta. We hypothesised that both within- and transgenerational plasticity would induce phenotypic changes associated with differential gene expression. Our results confirmed within- and transgenerational plasticity: F1 snails respond to predator-cue exposure by increasing escape behaviour, reducing shell length, and developing thicker and slenderer shells, whereas F2 snails from exposed parents have longer and thicker shells with narrower apertures. Within- and transgenerational plasticity were accompanied by the differential expression of 112 genes (101 up- and 11 downregulated) and 23 differentially expressed genes (17 up- and 6 downregulated), respectively. Within- and transgenerational plasticity did not share common differentially expressed genes, but the associated molecular functions, involving metabolism and transcription regulation, were similar. These results suggest that predator-induced within-generational plasticity and transgenerational plasticity may result from different genomic pathways and may evolve independently.
对捕食风险作出反应的诱导防御是适应性表型可塑性的一个著名例子。尽管诱导防御主要是在一个世代内进行研究（代内可塑性），但现在有明确证据表明，即使后代自身未接触过捕食风险，其祖先接触捕食风险也会影响后代所表现出的防御（跨代可塑性）。目前对允许环境信息跨代传递的分子机制还了解甚少。在本研究中，我们将淡水螺尖膀胱螺两代的反捕食反应（行为和形态）测量与转录组学研究相结合。我们假设代内和跨代可塑性都会诱导与基因表达差异相关的表型变化。我们结果证实了代内和跨代可塑性：F1代螺对捕食者线索暴露的反应是增加逃逸行为、减小壳长，并发育出更厚且更细长的壳，而来自暴露亲本的F2代螺则具有更长、更厚且孔口更窄的壳。代内和跨代可塑性分别伴随着112个基因（101个上调和11个下调）和23个差异表达基因（17个上调和6个下调）的差异表达。代内和跨代可塑性没有共同的差异表达基因，但涉及代谢和转录调控的相关分子功能是相似的。这些结果表明，捕食者诱导的代内可塑性和跨代可塑性可能源于不同的基因组途径，并且可能独立进化。
