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PROVIDER: PRJDB20023 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Histone H3K9 acetylation enrichment is less conserved in intergenic regions than in promoters of cloned mice (CBX65)
| PRJDB20042 | ENA
Project description:Genome-Wide Analysis of H3K9 Acetylation in THP-1
| PRJDB14412 | ENA
Project description:Somatic cell nuclear transfer has brought considerable chances to breed excellent breeds and protect endanger animals, while also produced numerous fail embryos and abnormal individuals due to inefficient epigenetic modification at the same time. To understand some mechanisms of abnormal piglets with phenotypes such as macroglossia, standing and walking disabilities in our study and find some differences between abnormal piglets and conventionally bred normal piglets, DNA methylation profile and genome-wide gene expression were conducted in two groups, using methylated DNA immunoprecipitation binding highthroughput sequencing (MeDIP-Seq) and RNA sequencing(RNA-Seq). We generated and provided a genome-wide DNA methylation and gene expression profile for abnormal cloned and conventionally bred piglets. We detected a total of 1493 genes differentially expressed in two groups and 382 of these genes also differentially methylated in two groups. Analysis of relationship between DNA methylation and gene expression revealed that DNA methylation levels had significantly negative and monotonic correlation with gene expression levels in particular regions of genes while no obvious monotonic correlation in other regions. Besides, we found some interesting genes and pathways such as MYH7 and mTOR signalling pathway that may played essential role in muscle growth and development. Briefly, these results provide reliable data for future epigenetic studies and may help to uncover the mechanism of failure clones via SCNT. We dissected the leg muscle from the cloned piglets and the conventionally bred piglets, and analyzed the difference of MeDIP-seq and RNA-seq between the two groups. As for data of abnormal cloned piglets, we downloaded it from GEO under Super-Series accession No. GSE51477, including SubSeries accession No.GSE51282 for RNA-seq data (No. GSM1241829 for abnormal cloned group) and SubSeries accession No. GSE51476 for MeDIP-seq data (No. GSM1246252 for abnormal cloned group).
2016-02-26 | E-GEOD-70004 | biostudies-arrayexpress
Project description:Genome-wide maps of the H3K9 acetylation state in embryonic stem cells (ESCs) before and after treatment with low levels of the histone deacetylase (HDAC) inhibitor valproic acid (VPA).
2011-09-17 | GSE24211 | GEO
Project description:Abnormal placentation in cloned animals remains an unsolved problem. We demonstrated the involvement of micro RNAs (miRNAs) in the abnormal enlargement (hyperplasia) of placentas in cloned mice. Using a comparative transcriptome analysis of cloned placentas, we noted the consistent upregulation of clustered miRNAs within Sfmbt2, a paternally expressed imprinted gene. This region was biallelically activated by loss of imprinting (LOI) in cloned placentas. Deletion of the maternal allele of the whole miRNA cluster resulted in the correction of their expression levels and upregulation of their putative target genes with antitumor or apoptotic functions. Consequently, the placental size was reduced to the normal level and histology was ameliorated. In contrast, correcting the expression of the LOI genes (Sfmbt2, Gab1, and Scl38a4) in cloned placentas had no impact on placental size. Thus, we identified that LOI of clustered miRNAs within Sfmbt2 in cloned placentas was the major cause of abnormal placental enlargement.
2020-02-29 | GSE129541 | GEO
Project description:Genome-wide profiling of H3K9/K14 Acetylation and H3K27 trimethylation at promoters in the human lung embryonic fibroblast cell line MRC5
2013-11-11 | E-MTAB-2004 | biostudies-arrayexpress
Project description:Transcription regulation in pluripotent embryonic stem (ES) cells is a complex process that involves multitude of regulatory layers, one of which is post-translational modification of histones. Here we have investigated the genome-wide occurrence of two histone marks, acetylation of histone H3K9 and K14 (H3K9ac and H3K14ac), in mouse ES cells. We demonstrate genome-wide that H3K9ac and H3K14ac show very high correlation. Examination of H3K9ac and H3K14ac in mES cells
2012-10-01 | E-GEOD-31284 | biostudies-arrayexpress
Project description:Backgroud:Epigenetic modifications (especially altered DNA methylation) resulting in altered gene expression may be one reason for development failure or the abnormality of the cloned animals, but the underlying mechanism of the abnormal phenotype in the cloned piglets remains unrevealed. Some cloned piglets in our study showed abnormal phenotypes such as big tongue (longer and thicker), limp, and exomphalos, which is similar to the human BWS syndrome. Here we conducted DNA methylation (DNAm) immunoprecipitation binding high throughput sequencing (MeDIP-seq) and RNA sequencing (RNA-seq) of muscle tissues of cloned piglets to investigate the relationship of abnormal DNAm with gene dysregulation and the unusual phenotypes in cloned piglets. Results:Analysis of the methylomes revealed that abnormal cloned piglets suffered more hypomethylated differentially methylated regions (DMRs) than hypermethylated DMRs compared to the normal cloned piglets. The DNAm level in the CpG Island was higher in the abnormal cloned piglets. Some repetitive elements, such as SINE/tRNA-Glu Satellite/centr also showed significant differences. Besides we detected 1,711 differentially expressed genes (DEGs) between the two groups, of which 243 genes also changed methylation level in the abnormal cloned piglets. The altered DNA methylation mainly affected the low and silent expression genes. We also found some interesting pathways and genes, such as MAPK signalling pathway, hypertrophic cardiomyopathy pathway, TPM3 gene and the imprinted gene PLAGL1, which may played important roles in the abnormal phenotype development. Conclusions;The abnormal cloned piglets showed substantial change both in the DNAm and the gene expression levels. Our data may provide new insights into understanding the molecular mechanisms of the reprogramming of genetic information in cloned animals. We dissected the biceps femoris muscle from the abnormal cloned piglets and the normal cloned piglets, and analyzed the difference of MeDIP-seq and RNA-seq between the two groups.
2014-09-03 | E-GEOD-51476 | biostudies-arrayexpress
Project description:Genome-wide maps of the H3K9 acetylation state in embryonic stem cells (ESCs) before and after treatment with low levels of the histone deacetylase (HDAC) inhibitor valproic acid (VPA). ChIP-seq for 3 samples: untreated E14 cells, cells treated with VPA for 4 hrs and cells treated with VPA for 16 hrs. Unprecipitated DNA was used as the input control (Input).
2011-09-17 | E-GEOD-24211 | biostudies-arrayexpress
Project description:Pharmacological treatment of Duchenne Muscular Dystrophy (DMD) with histone deacetylase inhibitors (HDACi) is currently being tested in clinical trials. Pre-clinical studies performed in mdx mice - the mouse model of DMD - have shown that HDACi promote compensatory muscle regeneration, while inhibiting fibro-adipogenic degeneration, by targeting fibro-adipogenic progenitors (FAPs); however, these beneficial effects are restricted to early stages of disease progression. We show here that FAPs from late stage mdx mice exhibit epigenetic and transcriptional features of senescence that could not be fully reversed by HDACi. In particular, genome-wide increase in H3K9/14 acetylation at gene promoters of Senescence Associated Secretory Phenotype (SASP) genes was associated with their upregulation in late stage mdx FAPs. Treatment with the HDACi Trichostatin A (TSA) could inhibit SASP gene activation in FAPs, by decreasing H3K9/14 acetylation. Conversely, combinatorial decrease of H3K27 and/or H3K9/14 acetylation at promoters of genes required for cycle activation and progression was associated with their downregulation in FAPs from late stage mdx mice. However, these epigenetic and transcriptional alterations could not be reversed by TSA, due to a general resistance exhibited by FAPs from late stage mdx mice to HDACi-induced H3K9/14 hyperacetylation. Overall, this data reveal that disease-associated features of senescence develop in FAPs of DMD muscle through epigenetically distinct and pharmacologically dissociable events, and suggests that HDACi might at least retain anti- fibrotic and inflammatory activity at late stages of DMD, by repressing FAP-derived SASP.
2022-02-01 | GSE189823 | GEO