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Telomere Shortening Impairs PGC Fate Decision [RNA-seq]

ABSTRACT: Telomere Shortening Impairs PGC Fate Decision [RNA-seq]

PROVIDER: PRJNA660794 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12566511_1.fastq.gz	Fastqsanger.gz
	SRR12566511_2.fastq.gz	Fastqsanger.gz
	SRR12566512_1.fastq.gz	Fastqsanger.gz
	SRR12566512_2.fastq.gz	Fastqsanger.gz
	SRR12566513_1.fastq.gz	Fastqsanger.gz

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Telomere Shortening Impairs PGC Fate Decision

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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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Telomere Shortening Impairs PGC Fate Decision

Project description:This SuperSeries is composed of the SubSeries listed below.

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Telomere shortening is associated with over-expression of subtelomeric genesin thyroid tumors.

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Project description:Oxidative stress is a primary cause of cellular senescence and contributes to the pathogenesis of numerous human diseases. Oxidative damage to telomeric DNA is proposed to trigger premature senescence by accelerating telomere shortening. Here we tested this model directly using a precision tool to produce the common base lesion 8-oxoguanine (8oxoG) exclusively at telomeres in human fibroblast and epithelial cells. A single induction of telomeric 8oxoG is sufficient to trigger multiple hallmarks of p53-dependent senescence. Telomeric 8oxoG activates ATM and ATR signaling, and enriches for markers of telomere dysfunction in replicating, but not quiescent cells. Acute 8oxoG production fails to shorten telomeres, but rather generates fragile sites and delayed mitotic DNA synthesis at telomeres, indicative of impaired replication. Based on our results we propose that oxidative stress promotes rapid senescence by producing oxidative base lesions which drive replication-dependent telomere fragility and dysfunction in the absence of shortening and shelterin loss.

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