Immediate and delayed hypothalamic response to monochromatic green illumination during the avian embryonic period are mediated thorough epigenetic modulations
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ABSTRACT:
PROVIDER: PRJNA1141430 | ENA |
REPOSITORIES: ENA
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Project description:In this study, we investigated the effects of light-induced fetal responses in avian species, specifically focusing on green monochromatic illumination (GMI). Broiler eggs were exposed to GMI either throughout the entire incubation period (Green) or specifically during the final three days before hatching (G3D), with control groups incubated in dark or white light conditions. Unbiased genome-wide analyses at day of hatch (DOH) revealed significant transcriptional changes in the hypothalamus of the G3D group, highlighting over 500 differentially expressed genes. In parallel with these transcriptional changes, our epigenetic analysis revealed that GMI exposure in the G3D group resulted in increased binding of phosphorylated CREB1 (pCREB1) and elevated levels of Histone H3 Lysine 27 acetylation (H3K27ac) at gene promoters linked to growth, appetite, and metabolism. Mechanistically, we found that pre-exposure to blue light, which disrupts green photoreceptor activity, reduced retinal green opsin levels and nullified the epigenetic modifications typically induced by GMI in the G3D group. Phenotypically, the G3D group exhibited increased post-hatch body weight at several stages, suggesting enhanced growth plasticity and metabolic efficiency, though these effects diminished with age. This study underscores the significant role of specific wavelengths and timing of light exposure in shaping developmental trajectories, and highlight the crucial role of epigenetics in shaping organismal responses to their environment.
2025-07-16 | GSE273328 | GEO
Project description:Objective: This study aimed to identify the transcriptome profiles from periodontal tissues of replanted teeth and evaluate the functional differences of transcriptomes between immediate replantation and delayed replantation in a rat teeth avulsion animal model. Background: In dental avulsion, the prognosis of replanted teeth is hardly favorable in delayed replantation. After tooth replantation, complex inflammatory responses occur to return homeostasis in periodontal tissue. Various types of cytokines are produced in inflammatory microenvironment and these cytokines determine the periodontal tissue responses. Methods: Maxillary first molars of Sprague–Dawley rats were extracted and exposed to dry environment, then replanted. The animals were divided into two groups according to extra–oral time: immediate replantation group (dry for 5 min) and delayed replantation (dry for 60 min). Either 3 or 7 days after replantation, the animals were sacrificed. The palatal gingival tissues were harvested for mRNA–sequencing. Hallmark gene set enrichment analysis were performed to predict the function of transcriptomes. Normalized enrichment score (NES) was generated to determine the functional differences between the groups. Results: Hallmark gene sets enriched in delayed replantation at 3 days were oxidative phosphorylation (NES=2.82, q < 0.001) and TNF–α signaling via NF–κB pathway (NES= 1.52, q=0.034). At 7 days, TNF–α signaling via NF–κB pathway (NES=–1.82, q=0.002), angiogenesis (NES=–1.66, q =0.01), and TGF–β signaling pathway (NES=–1.46, q=0.051) were negatively highlighted in delayed replantation compared to immediate replantation. Conclusions: Transcriptome profiles were significantly different between immediate replantation and delayed replantation. The responses of periodontal tissues were associated with TNF–α signaling via NF–κB pathway. However, the enrichment score of this pathway were changed with time–dependent manner between immediate replantation and delayed replantation.
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Project description:Peripheral nerve injuries represent a significant clinical challenge due to their limited regenerative capacity. Surgical repair strategies include immediate nerve repair, performed shortly after injury, and delayed nerve repair, conducted after a prolonged period when primary intervention is not feasible. Understanding the molecular and genetic mechanisms underlying both strategies is essential for optimizing functional recovery. This study compares the transcriptional landscape of delayed and immediate nerve repair over time to elucidate key pathways involved in nerve regeneration. A rat model of sciatic nerve injury was used, where an 8-mm nerve gap was repaired using a chitosan conduit either immediately or after a 3-month delay. Regenerated nerves were collected at 7-, 14-, and 21-days post-repair. RNA sequencing was performed to analyze transcriptomic changes across time points, and differentially expressed genes were identified and subjected to Gene Ontology enrichment analysis to identify functional pathways and regulatory networks involved in nerve regeneration. Distinct transcriptional profiles were observed across time points after immediate and delayed repair when comparing regenerating nerves with a healthy nerve. At 7 days, both exhibited a robust inflammatory response with upregulation of genes related to cytokine signaling and myeloid cell activation. By 14 days, many pathways related to response to lipoprotein particles and phagocytosis were upregulated, with delayed repair showing downregulation of myelination-associated genes. At 21 days, immune response activation, phagocytosis and lipoprotein particle activated pathways remained upregulated in both conditions. These findings suggest that immediate repair induces a faster regenerative response, whereas delayed repair follows a slower trajectory but engages similar molecular pathways. Despite initial differences, both strategies eventually converge on key regenerative mechanisms. These insights emphasize the benefits of early intervention while highlighting the potential for delayed repair to achieve functional recovery. Future research will focus on enhancing delayed repair outcomes through targeted molecular approaches.
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Project description:To identify putative regulatory elements enriched in the promoters of target genes of the PGE-dependent retrograde signaling pathway, we analyzed 500 bp regions of sequence upstream of genes whose expression was down-regulated by lincomycin. We treated dark-grown Arabidopsis seedlings with lincomycin, sampled them before or after a short illumination and examined the genomic response using Affymetrix ATH1 oligonucleotide microarrays. Differentially regulated genes were ranked based on descending degree of significance (p-value) and the top 50 genes affected by lincomycin in dark grown seedlings and top 50 genes affected by the antibiotic after illumination were selected for further analysis. Keywords: does response
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Project description:CosMx 6175 human gene for human kidney delayed graft function (DGF) and immediate graft function (IGF)
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Project description:Autophagy is a conserved catabolic process that plays an essential role under nutrient starvation condition and influences different developmental processes. We observed that seedlings of autophagy mutants (atg2, atg5, atg7, and atg9) germinated in the dark showed delayed chloroplast development following illumination. The delayed chloroplast development was characterized by a decrease in photosynthetic and chlorophyll biosynthetic proteins, lower chlorophyll content, reduced chloroplast size, and increased levels of proteins involved in lipid biosynthesis. Confirming the biological impact of these differences, photosynthetic performance was impaired in autophagy mutants 12h post illumination. We observed that while gene expression for photosynthetic machinery during de-etiolation was largely unaffected in atg mutants, several genes involved in photosystem assembly were transcriptionally downregulated. We also investigated if the delayed chloroplast development could be explained by lower lipid import to the chloroplast or lower triglyceride (TAG) turnover. We observed that the limitations in the chloroplast lipid import imposed by trigalactosyldiacylglycerol1 are unlikely to explain the delay in chloroplast development. However, we found that lower TAG mobility in the triacylglycerol lipase mutant sugardependent1 significantly affected de-etiolation. Moreover, we showed that lower levels of carbon resources exacerbated the slow-greening phenotype whereas higher levels of carbon resources had an opposite effect. This work suggests a lack of autophagy machinery limits chloroplast development during de-etiolation, and this is exacerbated by limited lipid turnover (lipophagy) that physically or energetically restrains chloroplast development.
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