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

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: GSE130780 | GEO | 2020/04/16

REPOSITORIES: GEO

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

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 | GSE146322 | 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 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 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 Shortening Impairs PGC Fate Decision [RNA-seq]

Project description:We asked whether telomere shortening impairs differentiation of ESCs into germ cell lineage. Terc-/- ESCs were used to investigate the effects of short telomeres on germ cell specification by in vitro differentiation. Short telomeres greatly reduced induction of PGCLCs from ESCs. Mechanistically, short telomeres resulted in excessive chromatin accessibility, which in turn activated the genes regulated by chromatin. Notably, Fst overexpression reduced BMP-Smad signaling and thus induction of PGCLCs, meanwhile upregulation of MAPK signaling pathway increase somatic lineage differentiation in short telomeres sampels. Moreover, knockin of Terc gene by CRISPR/Cas9 in Terc-/- ESCs restored telomere length and normal gene expression profile, and rescued PGCLC induction, revealing important roles of telomeres in PGC fate decision.

2022-08-31 | GSE157303 | GEO

Telomere Shortening Impairs PGC Fate Decision [ATAC-seq]

2022-08-31 | GSE157301 | GEO

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

2010-05-28 | GSE22016 | GEO

SIX1 cooperates with RUNX1 and SMAD4 in cell fate commitment of Mullerian duct epithelium.

Project description:During female mammal reproductive tract development, epithelial cells of the lower Müllerian duct are committed to become stratified squamous epithelium of the vagina and ectocervix, when the expression of ΔNp63 transcription factor is induced by mesenchymal cells. The absence of ΔNp63 expression leads to adenosis, the putative precursor of vaginal adenocarcinoma. Our previous studies with genetically engineered mouse models have established that fibroblast growth factor (FGF)/mitogen-activated protein kinase (MAPK), bone morphogenetic protein (BMP)/SMAD, and activin A/runt-related transcription factor 1 (RUNX1) signaling pathways are independently required for ΔNp63 expression in Müllerian duct epithelium (MDE). Here, we report that sine oculis homeobox homolog 1 (SIX1) plays a critical role in the activation of ΔNp63 locus in MDE as a downstream transcription factor of mesenchymal signals. In the developing mouse reproductive tract, SIX1 expression was restricted to MDE within the future cervix and vagina. SIX1 expression was totally absent in SMAD4 null MDE and was reduced in RUNX1 null and FGFR2 null MDE, indicating that SIX1 is under the control of vaginal mesenchymal factors: BMP4, activin A and FGF7/10. Furthermore, Six1, Runx1, and Smad4 gene-dose-dependently activated ΔNp63 expression in MDE within the vaginal fornix. Using a mouse model of diethylstilbestrol (DES)-associated vaginal adenosis, we found DES action through epithelial estrogen receptor α (ESR1) inhibits activation of ΔNp63 locus in MDE by transcriptionally repressing SIX1 and RUNX1 in the vaginal fornix.

| S-EPMC7852590 | biostudies-literature

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