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Methylation genes - BioProject

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Last Updated: 15 February 2022

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CG and CHG Methylation Contribute to the Transcriptional Control of OsPRR37-output Genes in Rice

With diurnal shifts of environmental cues, plant circadian clock coordinates endogenous transcriptional rhythms that coincide with plant circadian clock coordinates endogenous transcriptional rhythms. Rice growth and altered cytosine methylation in CG and CHG sequence contexts, but not in the CHH methylation context. We found that the overexpression of OsPRR37 reduced rice growth and altered cytosine methylation in CG and CHG sequence contexts, but not in the CHG methylation context. Both CG and CHG sites hypomethylated the promoter of OsHXK1's hexokinase gene OsHXK1 and CHG genes, and OsHXK1's expression was greatly elevated. In comparison, the leaf starch content in OsPRR37 overexpression lines was consistently lower in OsPRR37 overexpression lines than in the recipient's Guangluai 4. Around dusk, the genes involved in DNA methylation, methylation maintenance, and DNA demethylation were discovered to be on display. Our results revealed that CG and CHG methylation are linked to transcriptional control of OsPRR37-output genes, while hypomethylation of OsHXK1 leads to reduced rice production and delayed rice growth.

Source link: https://www.ncbi.nlm.nih.gov/bioproject/791371


Methotrexate treatment of newly diagnosed RA patients is associated with DNA methylation differences at genes relevant for disease pathogenesis and pharmacological action

After treatment with MTX, methylation changes in bulk T cells have been reported. Methotrexate is the first line therapy of rheumatoid arthritis, and methylation changes in bulk T cells have been documented. Cell-type specific DNA methylation changes in nave and memory CD4+ T cells have been investigated throughout the genome before and after MTX therapy of RA patients. Results: We discovered that MTX treatment had a significant effect on DNA methylation levels at several CpG sites in both cell populations. Interestingly, we found differentially methylated sites annotated to two genes; TRIM15 and SORC2, which have been used to predict treatment outcomes in RA patients when measured in bulk T cells. Conclusion: In CD4+ nave and memory T cells isolated from RA patients, we found CpG sites that were associated with MTX therapy. Overall, we've investigated cell-type specific DNA methylation changes in nave and memory CD4+ T cells before and after MTX treatment of RA patients.

Source link: https://www.ncbi.nlm.nih.gov/bioproject/779093


Perinatal exposure to nicotine alters spermatozoal DNA methylation near genes controlling nicotine action

The mechanism underlying chronic onset of perinatal smoke/nicotine-induced asthma is uncertain, but germline epigenetic modulations may play a role. We analyzed the DNA methylation pattern of spermatozoa of F1 rats exposed perinatally to nicotine in F0 gestation using a well-established rat model of perinatal nicotine-induced asthma. The top controlled gene body and promoter DMRs were tested for lung gene expression levels, and key proteins involved in lung growth and repair were determined. Introns, 5'UTRs, exons, introns, and 3'UTRs were not affected by nicotine use in F1 sperms, gene bodies, promoters, 5'UTRs, exons, introns, and 3'UTRs, and 3'UTRs. The mRNA expression and DNA methylation of gene expression were incongruous, according to gene expression analysis. The nicotine and placebo-treated groups were significantly different from the nicotine and placebo-treated groups. According to our results, DNA methylation in offspring spermatozoa has been remodeled in offspring spermatozoa after perinatal nicotine exposure. Sperm cells are isolated from the F1 generation.

Source link: https://www.ncbi.nlm.nih.gov/bioproject/727530


PRC1.6 and SETDB1-mediated repression of germline genes in the early embryo precedes DNA methylation-mediated silencing.

DNA methylation post-implantation is required for silencing of a subset of germline genes. H2K9me3's three ring1B-dependent H2AK119ub1 and H3K9me3 are enrich for RING1B-dependent H2K9me3 and H3K9me3 in embryos and nave ESCs. According to studies, silencing these genes in nESCs shows a greater dependency on PRC1. 6 than DNAme. In comparison, GGD genes are hypermethylated in epiblast-like cells, and their silencing is dependent on SETDB1, PRC1. 6/RING1B, and DNAme, with H3K9me3 and DNAme establishment dependent on MGA binding.

Source link: https://www.ncbi.nlm.nih.gov/bioproject/720611

* 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