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DNA methylation and demethylation.

DNA methylation and demethylation.

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The environment is closely related to the healthy rearing of animals. As an environmental stressor, heat stress has been paid close attention by practitioners. The high-temperature environment in summer will cause serious damage to poultry health and economic loss. As global temperatures rise, there is an urgent need for ways to mitigate heat stres...

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... the distal region of the promoter, CpG methylation prevents protein binding at these methylated sites, thus inhibiting gene transcription ( Kuroda et al. 2009). DNA demethylation depends on the ten-eleven translocation (TET) enzyme family, which can convert 5mc to 5hmc (5-hydroxymethylcytosine), which is an important intermediate in the demethylation process (Zhu, Stöger, and Alberio 2018) (Figure 1). Recently, Rosenberg et al. (2020) reported that the inhibition of TET enzyme activity at embryonic heat exposure by bis-2-(5-phenylacetamido-1,3,4-thiadiazol-2-yl) ethyl sulphide (BPTES) can enhance the inflammatory response of hypothalamus in chickens at the later stage of life, suggesting that TET enzyme plays an important role in the induction of hypothalamus heat tolerance during heat acclimation. ...

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... Epigenetic mechanisms, which include histone modification, DNA methylation [40], RNA driven gene regulation, chromatin remodeling, and post-transcriptional control, play crucial roles in genomic stability and function [41]. A wealth of evidence from epigenetic research studies in animals has demonstrated a crucial role for epigenetic mechanisms in modulating different biological pathways, such as heat resistance, adaptability, embryonic growth and development, immunity, and health [19,30,41,42]. The influence of epigenetic mechanisms on several critical functions at specific developmental stages or pathological conditions may be open to further research into the complex pathophysiology associated with infections or other important traits. ...
... In an earlier study, researchers [110] also reported significantly higher levels of HSP70 in the brain and liver of heat-adapted broiler chickens compared to a thermoneutral group. Additionally, an increase in HSP levels has been associated with various metabolic pathways involved in responding to heat stress [42]. Evidence from in silico studies indicates that HSP110, HSP90, and HSP70 are crucial for animal survival through transient increases in temperatures, where HSP78 and HSP60 contribute to survival during sustained periods of increased ambient temperatures [53]. ...
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There is increasing evidence indicating that global temperatures are rising significantly, a phenomenon commonly referred to as ‘global warming’, which in turn is believed to be causing drastic changes to the global climate. Global warming (GW) directly impacts animal health, reproduction, production, and welfare, presenting several challenges to livestock enterprises. Thermal stress (TS) is one of the key consequences of GW, and all animal species, including livestock, have diverse physiological, epigenetic and genetic mechanisms to respond to TS. As a result, TS can significantly affect an animals’ health, immune responsiveness, metabolic pathways etc. which can also influence the productivity, performance, and welfare of animals. Moreover, prolonged exposure to TS can lead to transgenerational and intergenerational changes that are mediated by epigenetic changes. For example, in several animal species, the effects of TS are encoded epigenetically during the animals’ growth or productive stage, and these epigenetic changes can be transmitted intergenerationally. Such epigenetic changes can affect animal productivity by changing the phenotype so that it aligns with its ancestors’ environment, irrespective of its immediate environment. Furthermore, epigenetic and genetic changes can also help protect cells from the adverse effects of TS by modulating the transcriptional status of heat-responsive genes in animals. This review focuses on the genetic and epigenetic modulation and regulation that occurs in TS conditions via HSPs, histone alterations and DNA methylation.
... Prenatal ambient temperature has been found to influence multiple epigenetic regulatory mechanisms (reviewed by Xu et al., 2022). Prenatal thermal challenge can influence histones, especially H3K4 methylation, associated with neurodevelopment in the hypothalamus of juvenile chickens (David et al., 2019), suggesting that neurogenesis could play a role in adaptation to heat stress later in life. ...
Article
Although the long-lasting effects of variation in early-life environment have been well documented across organisms, the underlying causal mechanisms are only recently starting to be unraveled. Yet understanding the underlying mechanisms of long-lasting effects can help us predict how organisms will respond to changing environments. Birds offer a great system in which to study developmental plasticity and its underlying mechanisms owing to the production of large external eggs and variation in developmental trajectories, combined with a long tradition of applied, physiological, ecological and evolutionary research. Epigenetic changes (such as DNA methylation) have been suggested to be a key mechanism mediating long-lasting effects of the early-life environment across taxa. More recently, changes in the early-life gut microbiome have been identified as another potential mediator of developmental plasticity. As a first step in understanding whether these mechanisms contribute to developmental plasticity in birds, this Review summarizes how changes in early-life environment (both prenatal and postnatal) influence epigenetic markers and the gut microbiome. The literature shows how both early-life biotic (such as resources and social environment) and abiotic (thermal environment and various anthropogenic stressors) factors modify epigenetic markers and the gut microbiome in birds, yet data concerning many other environmental factors are limited. The causal links of these modifications to lasting phenotypic changes are still scarce, but changes in the hypothalamic–pituitary–adrenal axis have been identified as one putative pathway. This Review identifies several knowledge gaps, including data on the long-term effects, stability of the molecular changes, and lack of diversity in the systems studied, and provides directions for future research.
... Based on the published reports and our extensive experiences with thermal stress in chickens, we selected a series of markers related to heat shock protein-related genes (HSF3, HSP70, HSPH1, and HSPD1, antioxidants (SOD1, SOD2, TXN, GPX1, GPX3, and NFE2L2) (Al-Zghoul, 2018), nutrient transporters (SLC3A1 and SLC6A14) and metabolism (FBP1, ACP6, FOXO1, and DIO3) , and growth-related genes (IGF1, IGF1R, IGF2, and GHR) (Loyau et al., 2014) in the liver. To comprehensively understand the TM in the brain, we analyzed some key markers for heat shock protein-related genes, antioxidants, thermoregulation (TRPV1, TRPV2, TRPV3, TRPA1, Eif2b45, CREB1, CRHR1, and CRHR2), and epigenetics (DNMT3A, DNMT3B, TDG, Gadd45B, EZH2, and H3k27) (Xu et al., 2022). ...
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The broilers’ health and growth performance are affected by egg quality, incubation conditions, and posthatch management. Broilers are more susceptible to heat stress because they have poor thermoregulatory capacity. So, it is crucial to develop a strategy to make chicks thermotolerant and cope with heat stress in post-hatch life. This study investigated the effects of embryonic thermal manipulation (TM) on different hatching parameters (hatch time, hatchability, and hatch weight), brain thermotolerance, and liver metabolism. Six hundred fertile Cobb 500 eggs were incubated for 21 d. After candling on embryonic day (ED) 10, 238 eggs were thermally manipulated at 38.5°C with 55% relative humidity (RH) from ED 12 to 18, then transferred to the hatcher (ED 19–21, standard temperature, 37.5°C) and 236 eggs were incubated at a standard temperature (37.5°C) till hatch. The samples were collected from the Control and TM groups on ED 15 and 18 of the embryonic periods. Hatchability was significantly higher (P < 0.05) in the TM group (94.50%) than in the control group (91.0%). Hatch weight did not differ significantly between the TM group (50.54 g) and the Control group (50.39 g). Most importantly, hatch time was significantly lower (P < 0.05) in the TM group than in the Control. In the D15 embryo brain, the mRNA expression of TRPV1,TRPV2, TRPV3, and the epigenetic marker H3K27 were significantly lower (P < 0.05) in the TM group compared to the Control group. However, in the D18 brain, the expression of TRPV1, TRPV2, and CRHR1 was significantly higher (P < 0.05) in the TM group than in the Control group. In the liver, the mRNA expression of SLC6A14 was significantly lower (P < 0.05) in the D15 TM group than in the D15 Control group. Conversely, the DIO3 mRNA expression was significantly higher (P < 0.05) in the D15 TM group than in the D15 Control group. The expression of GPX3, FOXO1, IGF2, and GHR in the liver was significantly higher in the D18 TM group compared to the D18 Control group (P < 0.05). In conclusion, increased expression of the aforementioned markers during the later embryonic period has been linked to reduced hatch time by increasing liver metabolism and thermotolerance capacity in the brain.
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This study was conducted to investigate the effect of in ovo betaine (IOB) and thermal manipulation during incubation on growth performance, and some immune parameters of broilers under cyclic heat stress (CHS). Eggs were incubated under control (CL) and heat acclimation (HA) conditions. Betaine was injected into chicken embryos at day 11 of incubation (E11). Chicks were raised under standard management conditions until 21 d of age. From 21 to 42 d of age, half of the birds from each incubation treatment (IT) were exposed to CHS. The others were kept at 24°C (OPT). Betain and HA did not affect embryonic mortalities, hatchability, chick weight, and relative weights of digestive organs of chicks. Thymus and spleen weights of chicks increased with betain. The serum IgG was higher in HA + IOB-treated chicks. Blood cholesterol was not influenced by treatments. At 7 and 21 d, the body weights (BW) of chicks from IOB had heavier. At 28 and 35 d, there were significant interaction between IT × rearing temperature (RT) and IOB × RT on BW. Betain increased feed consumption (FC) and improved feed conversion (FCR) from 0 to 21 d. At 28 d, IT × RT interaction on FC was significant. At 35 d, there were significant interactions among IT × IOB × RT on FC and FCR. Betain slightly improved FCR from 0 to 42 d. These results indicated that HA and IOB positively affected thymus weight and IgG level of day-old chicks and enhanced broiler performance of birds under CHS.