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Telomeres suppress the activity of retrotransposons in pluripotent stem cells [exp1]

ABSTRACT: Telomeres, which locate at the end of chromosomes protect chromosomes from fusion and deterioration. This is essential for cells to maintain genome staibility. Hee, we applied RNA-seq, to identify the impact of Terc knockout on the expression of retrotransposons in embryonic stem cells. In addition, we performed ChIP-seq to identify changes of histone mark H3K9me3 after telomere shortening.

ORGANISM(S): Mus musculus

PROVIDER: GSE100168 | GEO | 2022/12/25

REPOSITORIES: GEO

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Telomeres suppress the activity of retrotransposons in pluripotent stem cells [exp2]

Project description:Telomeres, which locate at the end of chromosomes protect chromosomes from fusion and deterioration. This is essential for cells to maintain genome staibility. We applied RNA-seq, to identify the impact of Terc knockout on the expression of retrotransposons in embryonic stem cells.

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Telomeres suppress the activity of retrotransposons in pluripotent stem cells

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Differential gene expression profiles of long bones of telomerase deficient mice (G3-mTERC-/-)

Project description:Telomere shortening due to telomerase deficiency leads to accelerated senescence of human skeletal (mesenchymal) stem cells (MSC) in vitro. In order to study the role of telomere shortening in vivo, we studied the phenotype of telomerase deficient mice caused by absence of telomerase RNA component (TERC-/-). TERC-/- exhibited accelerated age-related bone loss starting at 3 months of age and during 12 months follow up. Bone histomorphometry revealed decreased mineralized surface and bone formation rate as well as increased osteoclast number and size in TERC-/-. Also, serum total deoxy-pyridinoline (tDPD) was increased in TERC-/-. MSC isolated from TERC-/- exhibited intrinsic defects with reduced total number, lower proliferation rate, decreased expression of osteoblastic (OB) differentiation markers and formed less in vivo ectopic bone compared to WT cells. The TERC-/--MSC cultures accumulated a larger proportion of senescent Ã-galactosidase+ cells and cells exhibiting DNA damage positive for Î³-H2AX. Micro-array analysis of bones of TERC-/- and WT revealed significant over-expression of a large number of pro-inflammatory genes and signaling pathways in TERC-/- known to control osteoclast (OC) differentiation. In accordance with that, serum from TERC-/- enhanced OC formation in control bone marrow cultures. Our data demonstrate two mechanisms for age-related bone loss caused by telomerase deficiency: intrinsic osteoblastic defects and creation of pro-inflammatory osteoclast-activating microenvironment. Approaches for re-telomerization of MSC may provide a novel approach for abolishing age-related bone loss. control (WT) and the test (G3 - mTERC-/-) samples

2010-05-27 | E-GEOD-21523 | biostudies-arrayexpress

Expression data between WT and G3/4 Terc KO mouse ESCs during differentiation

Project description:Mammalian telomeres are formed by tandem repeats of the TTAGGG sequence, and shorten with each round of cell division in the absence of telomerase. Telomere shortening and dysfunction has been implicated in the pathology of several age-related diseases and premature ageing syndromes. Telomerase is important for telomere length maintenance. Telomerase RNA component, also known as TERC, is a component of telomerase. Terc knockout leads to telomerase deficiency and telomere shortening. Heterozygous telomerase-deficient (Terc+/-) mice were housed and bred for homozygous generation. ESC lines were generated with high efficiency from wild-type (WT, Terc+/+), heterozygous (Het, Terc+/-) and early- to late-generation (G1, G3 and G4) Terc-/- mouse blastocysts. Telomeres were shorter in Terc+/- ES cells than in WT ES cells, and further shortened from G1 to G4 Terc-/- ES cells. We took advantage of ES cell lines with various telomere lengths to investigate roles of telomere length on differentiation capacity of ES cells. We found that telomere length, but not telomerase activity, is required for differentiation of ES cells into epidermis. We performed microarray analysis to investigate differential gene expression profile at genome-wide levels between WT and G3/G4 Terc-/- (KO) mouse ES cells and during differentiation in vitro of WT and G4 Terc-/- mouse ES cells.

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Differential gene expression profiles of long bones of telomerase deficient mice (G3-mTERC-/-)

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The mTOR pathway is necessary for survival of mice with short telomeres.

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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.

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