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Differentiation Shifts from a Reversible to an Irreversible Heterochromatin State at the DM1 locus

ABSTRACT: Differentiation Shifts from a Reversible to an Irreversible Heterochromatin State at the DM1 locus

PROVIDER: PRJNA529246 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26959279.fastq.gz	Fastqsanger.gz
	SRR26959280.fastq.gz	Fastqsanger.gz
	SRR26959281.fastq.gz	Fastqsanger.gz
	SRR26959282.fastq.gz	Fastqsanger.gz
	SRR26959283.fastq.gz	Fastqsanger.gz

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Differentiation Shifts from a Reversible to an Irreversible Heterochromatin State at the DM1 locus

Project description:Epigenetic defects caused by hereditary or de novo mutations are implicated in various human diseases. It remains uncertain whether correcting the underlying mutation can reverse these defects in patient cells. Focusing on myotonic dystrophy type 1 (DM1), we discovered a fundamental difference between undifferentiated and differentiated cells. While in mutant human embryonic stem cells (hESCs), DNA methylation and H3K9me3 enrichments are completely abolished by repeat excision (2000CTG), in patients' myoblasts (CTG2600 expansion) repeat deletion fails to do so. This distinction stems from cell differentiation, and can be set back by reprogramming gene-edited myoblasts. We demonstrate that abnormal methylation in DM1 is distinctively maintained in the undifferentiated state by the activity of the de novo DNMTs (DNMT3b and/or DNMT3a). Overall, these findings highlight a crucial difference in heterochromatin maintenance between undifferentiated (sequence-dependent) and differentiated (sequence-independent) cells, underscoring the role of differentiation as a locking mechanism for repressive epigenetic modifications at the DM1 locus.

2024-02-06 | GSE128901 | GEO

Differentiation shifts from a reversible to an irreversible heterochromatin state at the DM1 locus.

Project description:Epigenetic defects caused by hereditary or de novo mutations are implicated in various human diseases. It remains uncertain whether correcting the underlying mutation can reverse these defects in patient cells. Here we show by the analysis of myotonic dystrophy type 1 (DM1)-related locus that in mutant human embryonic stem cells (hESCs), DNA methylation and H3K9me3 enrichments are completely abolished by repeat excision (CTG2000 expansion), whereas in patient myoblasts (CTG2600 expansion), repeat deletion fails to do so. This distinction between undifferentiated and differentiated cells arises during cell differentiation, and can be reversed by reprogramming of gene-edited myoblasts. We demonstrate that abnormal methylation in DM1 is distinctively maintained in the undifferentiated state by the activity of the de novo DNMTs (DNMT3b in tandem with DNMT3a). Overall, the findings highlight a crucial difference in heterochromatin maintenance between undifferentiated (sequence-dependent) and differentiated (sequence-independent) cells, thus underscoring the role of differentiation as a locking mechanism for repressive epigenetic modifications at the DM1 locus.

| S-EPMC11021500 | biostudies-literature

Reversible and irreversible anchorage independent growth in skin cells

Project description:We have investigated the regulation of anchorage-independent growth (AIG) by basic fibroblast growth factor (bFGF) and 12-O-tetradecanoyl phorbol-13-acetate (TPA) in JB6 mouse epidermal cells in the context of wound repair versus carcinogenesis responses. bFGF induces an unusually efficient but reversible AIG response, relative to TPA-induced AIG which is irreversible. Distinct global gene expression profiles are associated with anchorage-independent colonies arising from bFGF-stimulated JB6 cells, relative to colonies arising from fully tumorigenic JB6 cells (RT101), including genes exhibiting reciprocal regulation patterns. Thus, while TPA exposure results in commitment to an irreversible and tumorigenic AIG phenotype, the AIG response to bFGF is reversible with essentially complete restoration of normal cell cycle check point control following removal of bFGF from growth medium. These results are consistent with the physiological role of bFGF in promoting wound healing, and suggest that natural mechanisms exist to reverse transformative cellular phenotypes associated with carcinogenesis. Keywords: cell phenotype comparison

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Expression data from normal or DM1 myoblasts

Project description:We are investigating the transcriptional response of changes in RNA steady-state levels between normal and DM1. We used microarrays to detail the global programme of gene expression differences in normal or DM1 myoblasts. Keywords: comparison Two types of cells were analyzed, normal or DM1 deficient. The expression differences were compared to each other and we have deciphered a gene expression profile that is representative of DM1 deficiency.

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