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RNA-Seq of early passage wild type and short telomere G1 G4 Terc-/- ESCs.

ABSTRACT: We aimed to investigate the retrotranspositon expression after telomere shortening.

ORGANISM(S): Mus musculus

PROVIDER: GSE192876 | GEO | 2022/01/04

REPOSITORIES: GEO

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RNA-Seq of early passage wild type and short telomere G1 G4 Terc-/- ESCs.

Project description:RNA-Seq of early passage wild type and short telomere G1 G4 Terc-/- ESCs.

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

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Project description:The telomerase RNA component (TERC) is a critical determinant of cellular self renewal. Poly(A)-specific ribonuclease (PARN) is required for post-transcriptional maturation of TERC. PARN mutations lead to incomplete 3â² end processing and increased destruction of nascent TERC RNA transcripts, resulting in telomerase deficiency and telomere diseases. Here, we determined that overexpression of TERC increased telomere length in PARN-deficient cells and hypothesized that decreasing post-transcriptional 3â² oligo-adenylation of TERC would counteract the deleterious effects of PARN mutations. Inhibition of the noncanonical poly(A) polymerase PAP-associated domainâcontaining 5 (PAPD5) increased TERC levels in PARN-mutant patient cells. PAPD5 inhibition was also associated with increases in TERC stability, telomerase activity, and telomere elongation. Our results demonstrate that manipulating post-transcriptional regulatory pathways may be a potential strategy to reverse the molecular hallmarks of telomere disease. mRNA sequencing of induced pluripotent stem cells and 293 cell line.

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RNA-Seq of wild type and Terc-/- in G3 tail, G3 liver, G3 testis, G3 TTF, G3 ASC, G4 early ESC, G4 late ESC

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Project description:The telomerase RNA component (TERC) is a critical determinant of cellular self renewal. Poly(A)-specific ribonuclease (PARN) is required for post-transcriptional maturation of TERC. PARN mutations lead to incomplete 3′ end processing and increased destruction of nascent TERC RNA transcripts, resulting in telomerase deficiency and telomere diseases. Here, we determined that overexpression of TERC increased telomere length in PARN-deficient cells and hypothesized that decreasing post-transcriptional 3′ oligo-adenylation of TERC would counteract the deleterious effects of PARN mutations. Inhibition of the noncanonical poly(A) polymerase PAP-associated domain–containing 5 (PAPD5) increased TERC levels in PARN-mutant patient cells. PAPD5 inhibition was also associated with increases in TERC stability, telomerase activity, and telomere elongation. Our results demonstrate that manipulating post-transcriptional regulatory pathways may be a potential strategy to reverse the molecular hallmarks of telomere disease.

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