Integrative analyses of differential gene expression and DNA methylation of ethylbenzene-exposed workers

2015 ◽  
Vol 9 (3) ◽  
pp. 259-267 ◽  
Author(s):  
Gi Won Kim ◽  
Ji Young Hong ◽  
So-Yeon Yu ◽  
Jeong Jin Ahn ◽  
Youngjoo Kim ◽  
...  
2021 ◽  
Author(s):  
Carlos A. M. Cardoso-Junior ◽  
Boris Yagound ◽  
Isobel Ronai ◽  
Emily J. Remnant ◽  
Klaus Hartfelder ◽  
...  

AbstractIntragenic DNA methylation, also called gene body methylation, is an evolutionarily-conserved epigenetic mechanism in animals and plants. In social insects, gene body methylation is thought to contribute to behavioral plasticity, for example between foragers and nurse workers, by modulating gene expression. However, recent studies have suggested that the majority of DNA methylation is sequence-specific, and therefore cannot act as a flexible mediator between environmental cues and gene expression. To address this paradox, we examined whole-genome methylation patterns in the brains and ovaries of young honey bee workers that had been subjected to divergent social contexts: the presence or absence of the queen. Although these social contexts are known to bring about extreme changes in behavioral and reproductive traits through differential gene expression, we found no significant differences between the methylomes of workers from queenright and queenless colonies. In contrast, thousands of regions were differentially methylated between colonies, and these differences were not associated with differential gene expression in a subset of genes examined. Methylation patterns were highly similar between brain and ovary tissues and only differed in nine regions. These results strongly indicate that DNA methylation is not a driver of differential gene expression between tissues or behavioral morphs. Finally, despite the lack of difference in methylation patterns, queen presence affected the expression of all four DNA methyltransferase genes, suggesting that these enzymes have roles beyond DNA methylation. Therefore, the functional role of DNA methylation in social insect genomes remains an open question.


Diabetes ◽  
2011 ◽  
Vol 61 (2) ◽  
pp. 391-400 ◽  
Author(s):  
A. Groom ◽  
C. Potter ◽  
D. C. Swan ◽  
G. Fatemifar ◽  
D. M. Evans ◽  
...  

Author(s):  
Giovanna Rotondo Dottore ◽  
Ilaria Bucci ◽  
Giulia Lanzolla ◽  
Iacopo Dallan ◽  
Angela Sframeli ◽  
...  

Abstract Context Graves’ orbitopathy (GO) is an autoimmune disease that persists when immunosuppression is achieved. Orbital fibroblasts from GO patients display peculiar phenotypes even if not exposed to autoimmunity, possibly reflecting genetic or epigenetic mechanisms, which we investigated here. Objective We aimed to explore potential genetic or epigenetic differences using primary cultures of orbital fibroblasts from GO and control patients. Methods Cell proliferation, hyaluronic acid (HA) secretion, and HA synthases (HAS) were measured. Next-generation sequencing and gene expression analysis of the whole genome were performed, as well as real-time-PCR of selected genes and global DNA methylation assay on orbital fibroblasts from 6 patients with GO and 6 control patients from a referral center. Results Cell proliferation was higher in GO than in control fibroblasts. Likewise, HA in the cell medium was higher in GO fibroblasts. HAS-1 and HAS-2 did not differ between GO and control fibroblasts, whereas HAS-3 was more expressed in GO fibroblasts. No relevant gene variants were detected by whole-genome sequencing. However, 58 genes were found to be differentially expressed in GO compared with control fibroblasts, and RT-PCR confirmed the findings in 10 selected genes. We postulated that the differential gene expression was related to an epigenetic mechanism, reflecting diverse DNA methylation, which we therefore measured. In support of our hypothesis, global DNA methylation was significantly higher in GO fibroblasts. Conclusions We propose that, following an autoimmune insult, DNA methylation elicits differential gene expression and sustains the maintenance of GO.


2004 ◽  
Vol 24 (5) ◽  
pp. 1968-1982 ◽  
Author(s):  
Kotaro J. Kaneko ◽  
Theo Rein ◽  
Zong-Sheng Guo ◽  
Keith Latham ◽  
Melvin L. DePamphilis

ABSTRACT Soggy (Sgy) and Tead2, two closely linked genes with CpG islands, were coordinately expressed in mouse preimplantation embryos and embryonic stem (ES) cells but were differentially expressed in differentiated cells. Analysis of established cell lines revealed that Sgy gene expression could be fully repressed by methylation of the Sgy promoter and that DNA methylation acted synergistically with chromatin deacetylation. Differential gene expression correlated with differential DNA methylation, resulting in sharp transitions from methylated to unmethylated DNA at the open promoter in both normal cells and tissues, as well as in established cell lines. However, neither promoter was methylated in normal cells and tissues even when its transcripts were undetectable. Moreover, the Sgy promoter remained unmethylated as Sgy expression was repressed during ES cell differentiation. Therefore, DNA methylation was not the primary determinant of Sgy/Tead2 expression. Nevertheless, Sgy expression was consistently restricted to basal levels whenever downstream regulatory sequences were methylated, suggesting that DNA methylation restricts but does not regulate differential gene expression during mouse development.


2021 ◽  
Author(s):  
Natsuki Nakanishi ◽  
Satoko Osuka ◽  
Tomohiro Kono ◽  
Hisato Kobayashi ◽  
Shinya Ikeda ◽  
...  

Abstract Background: Polycystic ovary syndrome (PCOS), a common endocrinal disorder, is associated with impaired oocyte development, which leads to infertility. However, the pathogenesis of PCOS has not been completely elucidated. Limited studies have analyzed the pathological characteristics of oocytes in PCOS. This study aimed to analyze the differentially expressed genes (DEGs) and epigenetic changes in the oocytes of the PCOS mouse model to identify the etiological factors.Methods: C57BL/6J female mice were subcutaneously injected with vehicle or 5α-dihydrotestosterone (250 µg/day) on days 16–18 of pregnancy. Female offspring were used as the control or PCOS group. The oocytes were collected from mice aged 7–9 weeks. The DEGs between the control and PCOS groups were analyzed using RNA sequencing (RNA-Seq). Additionally, the DNA methylation status was analyzed using the post-bisulfite adaptor tagging method. The ovarian tissue sections were stained with hematoxylin and eosin to examine the morphological changes. The proteins, Rps21 and Rpl36, were measured using immunostaining.Results: Compared with the control group, the PCOS group exhibited impaired estrous cycle and polycystic ovary-like morphology. RNA-Seq analysis revealed that 90 DEGs were upregulated and 27 DEGs were downregulated in the PCOS mouse model. DNA methylation analysis revealed 30 hypomethylated and 10 hypermethylated regions in the PCOS group. However, the DNA methylation status was not correlated with differential gene expression. The Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis revealed that five DEGs (Rps21, Rpl36, Rpl36a, Rpl37a, and Rpl22l1) were enriched in ribosome-related pathways. The immunohistochemical analysis revealed that the expression levels of Rps21 and Rpl36 were significantly upregulated in the PCOS mouse model.Conclusions: These results suggest that differential gene expression in the oocytes of the PCOS mouse model is related to impaired folliculogenesis. These findings improved our understanding of the pathogenesis of PCOS.


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