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Methylation - Springer Nature

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Last Updated: 23 April 2022

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Antenatal Steroids and Cord Blood T-cell Glucocorticoid Receptor DNA Methylation and Exon 1 Splicing

We investigated the possibility that exposing antenatal BMZ alters cord blood immune cell composition in association with altered DNA methylation, which was similarly expressed in cord blood CD4+ T-cells with Exon 1 transcripts of the glucocorticoid receptor gene. 51 participants in the Antenatal Late Preterm Steroids Trial received cord blood from 51 people, including 7 BMZ and 24 placebo. Between BMZ and placebo, results of methylation at CpG sites in the GR promoter areas, and the expression of GR mRNA exon 1 variants were compared between BMZ and placebo.

Source link: https://doi.org/10.1007/s43032-022-00859-5


Immune checkpoint CD155 promoter methylation profiling reveals cancer-associated behaviors within breast neoplasia

Epigenetic DNA methylation shifts have been identified as key molecular mechanisms in cancer development. METHODS Methylation tests were carried out on 14 CpGs sites in the CD155 promoter area by bisulfite pyrosequencing. In multivariate analysis, Low CD155 methylation rates related to improved prognosis in univariate cox proportional hazard estimation and emerged as an independent predictor of survival in cox regression multivariate analysis. Further, methylation shifts at CD155 specific CpG sites were consistent with CD155 membranous mRNA isoform expression status, as shown by the number. When looking at the CpG7, CpG8, and CpG11 sites, statistical results revealed a significant connection with immune Natural Killer cell infiltrate. CONCLUSION ANALYSIS Our findings contribute to a better understanding of the effect of CD155 immune checkpoint modality expression in breast tumors, and we've reported for the first time that targeted CpG sites from CD155 promoter may be a potential biomarker for breast cancer surveillance.

Source link: https://doi.org/10.1007/s00262-021-03064-6


Global DNA methylation and cellular 5-methylcytosine and H4 acetylated patterns in primary and secondary dormant seeds of Capsella bursa-pastoris (L.) Medik. (shepherd’s purse)

Despite the importance of dormancy and dormancy cycling for plants' fitness and life cycle phenology, a comprehensive analysis of the global and cellular epigenetic trends in different seed dormancy states is lacking. Global DNA methylation levels in prolonged imbibed primary dormant seeds were highest in prolonged imbibed primary dormant seeds, with more 5-mC marked nuclei present only in specific regions of the seed. In secondary dormant seeds, global methylation rates, and 5-mC signals were higher at 3 and 7 days than 1 or 14 days. However, the RAM continued to show evidence after 14 days of imbibition under dormancy-inducing circumstances, suggesting a pivotal role for the radicle/RAM in the response to perceived environmental changes and the calibration of the seed dormancy state. We conclude that seed dormancy can be characterized by extensive gene modification that occurs in DNA methylation and H4 acetylation.

Source link: https://doi.org/10.1007/s00709-021-01678-2


Early DNA methylation changes in children developing beta cell autoimmunity at a young age

The aim of the study was to identify early DNA methylation changes associated with type 1 diabetes well before the diagnosis or even before the appearance of autoantibodies. Methods: Reduced representation bisulphite sequencing was used to investigate DNA methylation in purified CD4+ T cell, CD8+ T cell, and CD8+ CD8 cell fractions of 226 peripheral blood mononuclear cell samples longitudinally collected from seven type 1 diabetes-specific autoantibody-positive individuals and control individuals matched for age, sex, HLA risk, and place of birth. Using RNA sequencing results from the same samples, we also investigated correlations between DNA methylation and gene expression. Differential methylation in CD4+ T cells was found in pre-seroconversion samples at the very early stage of disease, including differential methylation at the promoter of IRF5 in CD4+ T cells.

Source link: https://doi.org/10.1007/s00125-022-05657-x


Epigenetic clock and methylation studies in marsupials: opossums, Tasmanian devils, kangaroos, and wallabies

We obtained DNA methylation data from n = 100 opossum samples from the ear, liver, and tail using the mammalian methylation array. We compared natal growth and later aging in the opossum methylome with those in mouse and other marsupial species such as Tasmanian devil, kangaroos, and wallabies. Although the opossum methylome is similar to that of mouse during postnatal development, it is different from that shared by other mammals in terms of the age-related rise in methylation at target sites of polycomb repressive complex 2. The human-opossum epigenetic clocks are expected to give opossum's attractiveness as a biological model. Additional epigenetic clocks for Tasmanian devil, red kangaroos, and other species of the genus Macropus may support species conservation efforts.

Source link: https://doi.org/10.1007/s11357-022-00569-5


The impact of NRG1 expressions and methylation on multifactorial Hirschsprung disease

HISTORY Hirschsprung disease is a complex genetic disorder characterized by the absence of ganglion cells in the intestines. According to a recent report, the NRG1 rare variant prevalence in Indonesian patients with HSCR is only 0. 9%. Methods This cross-sectional analysis found NRG1 type I, type II, and type III expressions in 20 patients with HSCR and ten control colons of 20 patients with HSCR and 10 control colons determined by real-time polymerase chain reaction. We treated the extracted gDNA from 16 HSCR patients' and 17 control colons with sodium bisulfate and analyzed the methylation pattern of NRG1 exon 1 with methylation-specific PCR. Conclusions Our research provides more insight into the aberrant NRG1 expression in patients with HSCR's colons, both ganglionic and aganglionic bowel, which may have a role in the production of HSCR, particularly in Indonesia.

Source link: https://doi.org/10.1186/s12887-022-03287-1


A pan-tissue DNA-methylation epigenetic clock based on deep learning

We collected 142 publicly available data sets from many human organs in order to create AltumAge, a neural network framework that is a highly accurate and precise age predictor. We then used deep learning modeling techniques to determine which methylation sites contributed to the final model predictions. Although most important CpG sites are linearly linked to age, some highly interacted CpG pages can also influence the quality of such links, as shown by the following table. We show that the CpG sites with the highest contribution to the model predictions were based on gene regulatory regions in the genome, including proximity to CTCF binding sites. Among other conditions, our neural network approach predicts higher age and cancer in tumor-related changes in vitro, such as immune and mitochondrial dysfunction, and HIV testing from patients with multiple sclerosis, type 2 diabetes, and HIV.

Source link: https://doi.org/10.1038/s41514-022-00085-y


Pioneer transcription factors are associated with the modulation of DNA methylation patterns across cancers

The aberrant DNA methylation patterns have been attributed to a lack of regulation of cancer cell-based regulation. We investigated the relationship between TF binding and DNA methylation in 19 cancer types by combining DNA methylation arrays and gene expression data with TF binding sites. We conducted emQTL tests in each cancer type and found 13 TFs whose expression levels were correlated with local DNA methylation patterns around their binding sites in at least two cancer types. In breast cancer MCF-7 cells, we experimentally demonstrated that FOXA1 knock-down is related to increased methylation in regions bound by FOXA1 in breast cancer MCF-7 cells, as an example. We also reported physical interactions between FOXA1 and TET1 and TET2 in vitro and in vivo at physiological rates in MCF-7 cells, providing additional encouragement to FOXA1's receptor for TET1 and TET2 to induce local demethylation in cancer cells.

Source link: https://doi.org/10.1186/s13072-022-00444-9


Aberrant promoter methylation contributes to LRIG1 silencing in basal/triple-negative breast cancer

In colorectal and cervical cancer, silencing of LRIG1 through promoter CpG island methylation has been reported, but breast cancer studies have been limited. Methods In silico analysis of human breast cancer patient data, we were able to show a correlation between DNA methylation and LRIG1 silencing in basal/triple-negative breast cancer patients, as well as its effect on patient survival. Whether in breast cancer cell lines in vitro, quantitative reverse-transcription PCR, protein abundance, and methylation enrichment were investigated by quantitative reverse-transcription PCR, immunoblotting, and methylation immunoprecipitation. We also investigated the consequences of targeted demethylation of the LRIG1 CpG island and transcriptional activation of LRIG1 expression using the RNA guided deadCas9 transactivation device. Result 1: Across breast cancer subtypes, LRIG1 expression is lowest in the basal/triple-negative subtype, so we investigated whether differential methylation could play a role in this. Interestingly, we find that LRIG1 CpG island methylation is most prominent in basal/triple-negative cell lines and patient samples. 5-aza-2'-deoxycytidine decreases methylation resulting in an increase in LRIG1 transcript expression in basal/triple-negative cell lines, but has no effect on LRIG1 expression in luminal/ER-positive cell lines. We show that TET1-mediated demethylation and VP64-mediated transcriptional activation at the CpG island led to an increase in endogenous LRIG1 expression in basal/triple-negative breast cancer cells, but not at predicted off-target sites, according to predicted transcriptional upregulation. For the first time, we report that our research contributes to a new understanding of the mechanisms that suppress LRIG1 in triple-negative breast cancer, and it shows that repressing LRIG1 in cancer cells is possible.

Source link: https://doi.org/10.1038/s41416-022-01812-8

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions