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Telomere dysfunction cooperates with epigenetic alterations to impair murine embryonic stem cell fate commitment II

ABSTRACT: This study demonstrates a specific cooperativity between perturbations in histone methylation and eroded telomeres to destabilize the differentiation of murine embryonic stem cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE146322 | GEO | 2020/04/16

REPOSITORIES: GEO

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Telomere dysfunction cooperates with epigenetic alterations to impair murine embryonic stem cell fate commitment

Project description:This study demonstrates a specific cooperativity between perturbations in histone methylation and eroded telomeres to destabilize the differentiation of murine embryonic stem cells.

2020-04-16 | GSE130780 | GEO

Telomere dysfunction cooperates with epigenetic alterations to impair murine embryonic stem cell fate commitment.

Project description:The precise relationship between epigenetic alterations and telomere dysfunction is still an extant question. Previously, we showed that eroded telomeres lead to differentiation instability in murine embryonic stem cells (mESCs) via DNA hypomethylation at pluripotency-factor promoters. Here, we uncovered that telomerase reverse transcriptase null (Tert-/-) mESCs exhibit genome-wide alterations in chromatin accessibility and gene expression during differentiation. These changes were accompanied by an increase of H3K27me3 globally, an altered chromatin landscape at the Pou5f1/Oct4 promoter, and a refractory response to differentiation cues. Inhibition of the Polycomb Repressive Complex 2 (PRC2), an H3K27 tri-methyltransferase, exacerbated the impairment in differentiation and pluripotency gene repression in Tert-/- mESCs but not wild-type mESCs, whereas inhibition of H3K27me3 demethylation led to a partial rescue of the Tert-/- phenotype. These data reveal a new interdependent relationship between H3K27me3 and telomere integrity in stem cell lineage commitment that may have implications in aging and cancer.

| S-EPMC7192583 | biostudies-literature

Telomere dysfunction and fusion during the progression of chronic lymphocytic leukaemia: evidence for a telomere crisis

Project description:We performed single-molecule telomere length and telomere fusion analysis in patients at different stages of chronic lymphocytic leukaemia (CLL). Our work identified the shortest telomeres ever recorded in primary human tissue reinforcing the concept that there is significant cell division in CLL. Furthermore, we provide direct evidence that critical telomere shortening, dysfunction and fusion contribute to disease progression. The frequency of short telomeres and fusion events increased with advanced disease, but importantly these were also found in a subset of early-stage patient samples indicating that these events can precede disease progression. Sequence analysis of fusion events isolated from individuals with the shortest telomeres revealed limited numbers of repeats at the breakpoint, sub-telomeric deletion and microhomology. Array-CGH analysis of individuals displaying evidence of telomere dysfunction revealed large-scale genomic rearrangements that were concentrated in the telomeric regions; this was not observed in samples with longer telomeres. Array CGH was undertaken on six individuals (five CLL stage C and one stage A) that displayed evidence of telomere dysfunction, and four (three CLL stage A and one stage B) that displayed longer and apparently stable telomeres.

2010-05-28 | E-GEOD-22016 | biostudies-arrayexpress

Telomere dysfunction induces Sirtuin repression that drives telomere-dependent disease

Project description:We have characterized the p53-dependent miRNAs in murine liver in telomerase knckout mice with short telomeres

2019-06-25 | GSE125847 | GEO

Telomere dysfunction and fusion during the progression of chronic lymphocytic leukaemia: evidence for a telomere crisis

2010-05-28 | GSE22016 | GEO

Telomere dysfunction cooperates with epigenetic alterations to impair murine embryonic stem cell fate commitment

Project description:Telomere dysfunction cooperates with epigenetic alterations to impair murine embryonic stem cell fate commitment

| PRJNA541428 | ENA

Telomere dysfunction cooperates with epigenetic alterations to impair murine embryonic stem cell fate commitment II

Project description:Telomere dysfunction cooperates with epigenetic alterations to impair murine embryonic stem cell fate commitment II

| PRJNA610082 | ENA

Telomere length effect on genes near the telomere in myoblasts

Project description:We examined differential expression of genes within 10MBs of telomeres in myoblasts with long or short telomeres We offer telomere looping with telomere length as a partial mechanistic explanation for the changes gene expression that is observed. Compare expression of genes within 10MB of the telomere in normal myoblasts with long (15 kb) and short (6 kb) telomeres.

2014-07-17 | E-GEOD-48973 | biostudies-arrayexpress

Expression data by telomere elongation

Project description:Limitless reproductive potential is one of the hallmarks of cancer cells1. This ability is accomplished by maintaining telomeres, which erosion otherwise causes cellular senescence or death. Human cancer cells often maintain shorter telomeres than do cells in surrounding normal tissues2-5. While most cancer cells activate telomerase, which can elongate telomeres6, it remains elusive why cancer cells keep telomeres short. Here we show that forced elongation of telomeres in cancer cells promotes their differentiation in a tumor microenvironment in vivo. We elongated telomeres of human prostate cancer PC-3 cells, which possess short telomeres7, by enhancing their telomerase activity. The resulting cells with long telomeres retain an ability to form tumors in a mouse xenograft model. Strikingly, these tumors exhibit many duct-like structures and reduced N-cadherin expression, reminiscent of well-differentiated adenocarcinoma. These phenotypic changes are caused by telomere elongation per se but not enhanced telomerase activity. Gene expression profiling revealed that telomere elongation correlates with inhibition of cell-cycle processes. Together, our results suggest a functional contribution of short telomeres to tumor malignancy by regulating cancer cell differentiation. Two samples are telomere-elongated cells, both in the presence and absence of the exogenous hTERT. The other two samples are control cell lines.

2013-05-31 | E-GEOD-36649 | biostudies-arrayexpress

Telomere length effect on genes near the telomere in myoblasts

2014-07-17 | GSE48973 | GEO