Transcriptional profiles of [ESI+]
Ontology highlight
ABSTRACT:
ORGANISM(S): Saccharomyces cerevisiae
PROVIDER: GSE117624 | GEO | 2020/02/29
REPOSITORIES: GEO
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Project description:We report the transcriptional profiles of the [ESI+] prion, as well as snt1∆, set3∆, and hos2∆ diploid cells.
2020-02-29 | GSE128672 | GEO
Project description:In this work, we studied function of rice DDM1 in coordinating DNA methylation, expression of small (sRNA) and long noncoding (lncRNA) RNAs, and nucleosome positioning by high throughput approaches.We show that the ddm1a/1b mutation resulted in ectopic CHH methylation of transposable elements (TE) and repeats. The ectopicCHH methylationwas dependent on DRM2, a DNA methyltransferase involved in sRNA-dependent DNA-methylation (RdDM). The ddm1a/1b mutation resulted in increases of heterochromatic sRNA but decreases of euchromatic sRNA production,induced expression of a set of developmentally regulated heterochromatic lncRNA , and increased nucleosome occupancy of TE-related or silent genes including heterochromatic lncRNA loci. In particular,DDM1-mediated repression ofCentromericRetrotransposons of Rice1 (CRR1) was essential for centromere function.
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Project description:Disappearance of the Barr body has long been considered a hallmark of cancer, although whether this corresponds to epigenetic instability and transcriptional reactivation, or to genetic loss, has remained unclear. Here we show that in breast cancer cell lines as well as primary breast tumors, the inactive X chromosome frequently displays a highly abnormal 3D nuclear organization, with global perturbations in its characteristic heterochromatic state, including apparent gain of euchromatic marks and lessening of repressive marks such as H3K27me3 and promoter DNA methylation. Genome-wide profiling of chromatin and transcription reveal modified epigenomic landscapes in cancer cells accompanied by a significant degree of X-linked gene reactivation, affecting genes previously implicated in cancer, including the histone deacetylase, HDAC8 and transducin (Beta)-Like 1X-Linked, TBL1X. We provide proof of principle that epigenetic deregulation can indeed perturb the dosage of some X-linked factors and demonstrate that many of these genes are reactivated in primary breast tumors. Our study establishes that the inactive X is subject to epigenetic erosion in a cancer context and sets the stage for the use of chromatin marks and X- chromosome genes as potential biomarkers to assess epigenetic changes in cancer. Examination of allele specific expression of genes using nascent RNA on snp6 array by comparing it with snp6 results from genomic DNA.
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Project description:Disappearance of the Barr body has long been considered a hallmark of cancer, although whether this corresponds to epigenetic instability and transcriptional reactivation, or to genetic loss, has remained unclear. Here we show that in breast cancer cell lines as well as primary breast tumors, the inactive X chromosome frequently displays a highly abnormal 3D nuclear organization, with global perturbations in its characteristic heterochromatic state, including apparent gain of euchromatic marks and lessening of repressive marks such as H3K27me3 and promoter DNA methylation. Genome-wide profiling of chromatin and transcription reveal modified epigenomic landscapes in cancer cells accompanied by a significant degree of X-linked gene reactivation, affecting genes previously implicated in cancer, including the histone deacetylase, HDAC8 and transducin (Beta)-Like 1X-Linked, TBL1X. We provide proof of principle that epigenetic deregulation can indeed perturb the dosage of some X-linked factors and demonstrate that many of these genes are reactivated in primary breast tumors. Our study establishes that the inactive X is subject to epigenetic erosion in a cancer context and sets the stage for the use of chromatin marks and X- chromosome genes as potential biomarkers to assess epigenetic changes in cancer. Examination of allele specific expression of genes in chrX using histone marks, transcriptome, exome and SNP data on two normal cell-line and three cancer cell-line.
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Project description:Transcriptional profiles of [ESI+]
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Project description:In budding yeast, Set2 catalyzes di- and trimethylation of H3K36 (H3K36me2 and H3K36me3) via an interaction between its SRI domain and C-terminal repeats of RNA polymerase II (Pol2) phosphorylated at Ser2 and Ser5 (CTD-S2,5-P). H3K36me2 recruits the Rpd3S histone deacetylase complex to repress cryptic transcription from transcribed regions. In fission yeast, Set2 is also responsible for H3K36 methylation, which represses a subset of RNAs including heterochromatic and subtelomeric RNAs, at least in part via recruitment of Clr6 complex II, a homolog of Rpd3S. Here, we show that CTD-S2Pâdependent interaction of fission yeast Set2 with Pol2 via the SRI domain is required for formation of H3K36me3, but not H3K36me2. H3K36me3 silenced heterochromatic and subtelomeric transcripts through post-transcriptional and transcriptional mechanisms, respectively, whereas H3K36me2 did not. Clr6 complex II appeared not to be responsible for heterochromatic silencing. Our results demonstrate that H3K36 methylation has multiple outputs in fission yeast; these findings provide insight into the multiple roles of H3K36 methylation in metazoans, which have different enzymes for synthesis of H3K36me1/2 and H3K36me3. Gene expression profile at exponentially-growing phase.in the fission yeast deletion mutants of set2.
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Project description:Eukaryotic DNA methylation is found in silent transposable elements and active genes. Nucleosome remodelers of the DDM1/Lsh family are thought to be specifically required to maintain transposon methylation, but the reason for this is unknown. Here, we find that a chromatin gradient that extends from the most heterochromatic transposons to euchromatic genes determines the requirement of DDM1 for methylation maintenance in all sequence contexts. We also show that small RNA-directed DNA methylation (RdDM) is inhibited by heterochromatin and absolutely requires the nucleosome remodeler DRD1. DDM1 and RdDM independently mediate nearly all transposon methylation, which is catalyzed by the methyltransferases MET1 (CG), CMT3 (CHG), DRM2 (CHH) and CMT2 (CHH), and collaborate to repress transposition and regulate the methylation and expression of genes. Our results indicate that the Arabidopsis genome is defined by a heterochromatic continuum that governs the access of DNA methyltransferases and potentially all DNA binding proteins. Examination of DNA methylation, transcription and nucleosomes in Arabidopsis wild-type and/or ddm1, RdDM and DNA methylase mutants.
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Project description:Epigenetic resetting in the mammalian germ line entailsacute DNA demethylation, which lays the foundation for gametogenesis, totipotency,and embryonic development. We characterize the epigenome of hypomethylated human primordial germ cells (hPGCs) to reveal mechanisms preventing the widespread derepression of genesand transposable elements (TEs). Along with the loss of DNA methylation, we show that hPGCsexhibit a profound reduction of repressive histone modifications resulting in diminished heterochromatic signaturesat most genesand TEsand the acquisition of a neutral or paused epigenetic state without transcriptional activation.Efficient maintenance of a heterochromatic state is limited to a subset of genomic loci, such asevolutionarily young TEsand some developmental genes, which require H3K9me3 and H3K27me3, respectively, forefficient transcriptional repression. Accordingly, transcriptional repression in hPGCs presentsan exemplary balanced system relying on local maintenance of heterochromatic featuresand a lack of inductive cues.
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