Evaluation of DNA methylation and mRNA expression of heat shock proteins in thermal manipulated chicken

Abstract

Thermal manipulation during embryogenesis has been demonstrated to enhance the thermotolerance capacity of broilers through epigenetic modifications. Heat shock proteins (HSPs) are induced in response to stress for guarding cells against damage. The present study investigates the effect of thermal conditioning during embryogenesis and thermal challenge at 42 days of age on HSP gene and protein expression, DNA methylation and in vitro luciferase assay in brain tissue of Naked Neck (NN) and Punjab Broiler-2 (PB-2) chicken. On the 15th day of incubation, fertile eggs from two breeds, NN and PB-2, were randomly divided in to two groups: control (C)-eggs were incubated under standard incubation conditions, and thermal conditioning (TC)-eggs were exposed to higher incubation temperature (40.5°C) for 3 h on the 15th, 16th, and 17th days of incubation. The chicks obtained from each group were further subdivided and reared under different environmental conditions from the 15th to the 42nd day as normal [N; 25 ± 1 °C, 70% relative humidity (RH)] and heat exposed (HE; 35 ± 1 °C, 50% RH) resulting in four treatment groups (CN, CHE, TCN, and TCHE). The results revealed that HSP promoter activity was stronger in CHE, which had lesser methylation and higher gene expression. The activity of promoter region was lesser in TCHE birds that were thermally manipulated at the embryonic stage, thus reflecting their stress-free condition. This was confirmed by the lower level of mRNA expression of all the HSP genes. In conclusion, thermal conditioning during embryogenesis has a positive impact and improves chicken thermotolerance capacity in postnatal life.

Avian ecological epigenetics: pitfalls and promises

“…We now know that epigenetic mechanisms contribute to phenotypic variation, and that these mechanisms are often active during development and can be altered in response to different environmental factors (Richards 2006), making them good candidates for the study of the mechanisms behind phenotypic plasticity. These environmental effects include chemicals that are present in the environment, like methyl donors (Weaver 2005), toxic substances (Romano et al 2017;Wallace et al 2018), or external factors such as incubation temperature (Vinoth et al 2018;Yan et al 2015) or maternal effects (Bentz et al 2016). Here, we discuss the role of epigenetic mechanisms in plastic changes within the concept of developmental plasticity, and refer to developmental plasticity as (an) irreversible change(s) in the phenotype resulting from environmentally introduced alterations of development, like early environmental effects (Forsman 2015), parasite load and anthropogenic effects.…”

Cross-talk between energy metabolism and epigenetics during temperature stress response in C2C12 myoblasts

“…Here, we analyzed the effects of temperature stress on different epigenetic modifications by comparing global DNA methylation and histone H4 acetylation, as well as the expression pattern of genes encoding various HDACs, HATs, DNMTs and TETs. Altered methylation in genes for heat shock proteins (HSPs) and corticotropinreleasing hormone, induced by heat stress during early embryonic stages, has an impact on the thermotolerance capacity in the postnatal life of broiler chickens [12,13]. We showed that, upon heat stress, C2C12 cells exhibited differential global DNA methylation compared to cells exposed to cold stress.…”

“…Genome-wide DNA methylation patterns are altered in the skeletal muscle of heat-stressed pigs [11]. Heat stress in postnatal stage (thermal conditioning) induces DNA methylation changes in the hypothalamicpituitary-adrenal axis which is involved in adaptation to heat load in adult chickens [12,13]. Key energy metabolites such as S-adenosylmethionine, acetyl CoA and ATP are essential for epigenetic modifications including DNA methylation and histone tail acetylation.…”

Embryonic canalization and its limits—A view from temperature

“…Differences in DNA methylation associated with different temperature regimes are well established (e.g., Ni et al, 2018; Pu & Zhan, 2017). Exposure of chick embryos to high temperature for short periods during embryonic development has long term consequences for resistance to deleterious effects of heat after hatching, and causes differences in methylation of heat shock promoters (Vinoth et al, 2018). In salmon, embryonic rearing temperature affected myogenin expression and corresponding levels of methyltransferases and DNA methylation (Burgerhout et al, 2017).…”