Abstract
Changes in gene activity through epigenetic alterations induced by early environmental challenges during embryogenesis are known to impact the phenotype, health, and disease risk of animals. Learning how environmental cues translate into persisting epigenetic memory may open new doors to improve robustness and resilience of developing animals. It has previously been shown that the heat tolerance of male broiler chickens was improved by cyclically elevating egg incubation temperature. The embryonic thermal manipulation enhanced gene expression response in muscle (P. major) when animals were heat challenged at slaughter age, 35 days post-hatch. However, the molecular mechanisms underlying this phenomenon remain unknown. Here, we investigated the genome-wide distribution, in hypothalamus and muscle tissues, of two histone post-translational modifications, H3K4me3 and H3K27me3, known to contribute to environmental memory in eukaryotes. We found 785 H3K4me3 and 148 H3K27me3 differential peaks in the hypothalamus, encompassing genes involved in neurodevelopmental, metabolic, and gene regulation functions. Interestingly, few differences were identified in the muscle tissue for which differential gene expression was previously described. These results demonstrate that the response to embryonic thermal manipulation (TM) in chicken is mediated, at least in part, by epigenetic changes in the hypothalamus that may contribute to the later-life thermal acclimation.
Highlights
During the last several decades, it became clear that the epigenome of eukaryotes dynamically responds to the environment
This study showed that several genes that code for components of the corticotropin-releasing hormone (CRH) signaling pathway were affected at the histone level, suggesting that thermal manipulation (TM) may affect biological processes similar to those affected by the postnatal acclimation model
TM was applied on Cob500 eggs and the reproducibility of the embryonic treatment was compared to previous experiments by measuring cloacal temperature at hatching, as this has been shown to be decreased in TM chickens (Loyau et al, 2015)
Summary
During the last several decades, it became clear that the epigenome of eukaryotes dynamically responds to the environment. Post-natal heat acclimation during the 3rd or 5th day of life was shown to improve temperature tolerance at 10 days of age through epigenetic changes such as DNA methylation at BDNF and histone post-translational modifications at BDNF, Eif2b5 and HSP70 in the hypothalamus (Yossifoff et al, 2008; Kisliouk et al, 2010; Kisliouk et al, 2011; Kisliouk et al, 2017). We hypothesized that an epigenetic reprogramming induced by the embryonic heat exposure may have modified part of the chromatin landscape affecting gene expression in favor of heat acclimation. To test this hypothesis, we performed a whole-genome analysis of H3K4me and H3K27me histone marks. This study showed that several genes that code for components of the corticotropin-releasing hormone (CRH) signaling pathway were affected at the histone level, suggesting that TM may affect biological processes similar to those affected by the postnatal acclimation model
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