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

ABSTRACT: Gene expression profiles of Terc+/+ and generation 2 (G2) Terc-/- male mice fed rapamycin or control diet during 2 months. Rapamycin diet contains encapsulated rapamycin at 42 ppm (mg of drug per kg of food); control diet contains coating material (Eudragit S100). Rapamycin was microencapsulated by Rapamycin Holdings Inc. (San Antonio, Texas) and was then incorporated into 5LG6 mouse chow (TestDiet, London, UK).

ORGANISM(S): Mus musculus

PROVIDER: GSE127475 | GEO | 2020/01/02

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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Telomerase subunit TERT regulates MYC stability independent of its role on telomeres (array)

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Project description:Constitutively active MYC and reactivated telomerase often co-exist in cancers. While the reactivation of telomerase is thought to be essential for replicative immortality, MYC, in conjunction with co-factors, confers several growth advantages to cancer cells. However, it is unclear which co-factors sustain elevated MYC activity in tumours . Here, we identify TERT, the catalytic subunit of telomerase, as a novel regulator of MYC stability in cancers. Binding of TERT to MYC stabilizes its levels on chromatin, contributing to either activation or repression of its target genes. Mechanistically, TERT regulates MYC ubiquitination and stability, and this effect of TERT is independent of its role on telomeres. Genetic inhibition and knocking out of TERT phenocopied the loss of MYC, resulting in reduced disease burden of early- and late-stage MYC-driven murine lymphomas. Conversly, the ectopic expression of TERT could substitute for reduced MYC in these functions. Finally we show that TERT null mice, unlike Terc null mice, show delayed onset of MYC induced lymphomagenesis. Accordingly, inhibiting TERT function in primary human leukemia cells blocked the expression of MYC targets, while Terc depletion had no effects . Based on our data, we conclude that the re-expression of TERT, a direct MYC target in tumors, provides a feed-forward mechanism to potentiate MYC-dependent oncogenesis. ChIP was performed using anti-MYC (sc-764) in primary lymphoma cells from Eµ-Myc;Tert -/- mice, Eµ-Myc;Tert +/+ mice, or in P493 cells treated with shTert, P493 shTerc and shControl.

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Telomerase subunit TERT regulates MYC stability independent of its role on telomeres (array)

2015-04-23 | GSE60175 | GEO

Telomerase subunit TERT regulates MYC stability independent of its role on telomeres (ChIP-Seq)

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