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Enhanced cardiac repair by human telomerase reverse transcriptase over-expression in human cardiac mesenchymal stem cells

ABSTRACT: Enhanced cardiac repair by human telomerase reverse transcriptase over-expression in human cardiac mesenchymal stem cells

PROVIDER: PRJNA445555 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6893020.fastq.gz	Fastqsanger.gz
	SRR6893030.fastq.gz	Fastqsanger.gz
	SRR6893040.fastq.gz	Fastqsanger.gz
	SRR6893021.fastq.gz	Fastqsanger.gz
	SRR6893031.fastq.gz	Fastqsanger.gz

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Enhanced cardiac repair by human telomerase reverse transcriptase over-expression in human cardiac mesenchymal stem cells

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Project description:Telomerase holoenzyme plays a critical role in maintaining telomere length, and thus in regulating inflammation caused by telomeric DNA damage. However, beyond its role in telomere maintenance, the molecular function of telomerase in directly regulating inflammation remains unclear. Here, we show that the reverse transcriptase component of telomerase, TERT, has a cell-type-specific role in directly regulating inflammation via the cytoplasmic cGAS-STING nucleic acid-sensing pathway. Analyses of murine and zebrafish models of gut inflammation and human colitis/Crohn’s patients document that this function of TERT is evolutionarily conserved. Using our novel knock-in TERTVAA mouse model where reverse-transcriptase-inactive TERT is driven by its endogenous loci, and molecular, pharmacological and single-cell approaches we identify the myeloid subpopulation, termed T-MAC, wherein TERT enhances STING activation and initiates type-1 interferon responses independent of reverse transcriptase activity or telomere length. We highlight a hitherto unappreciated role of TERT in directly regulating inflammation and provide a therapeutic rationale for targeting TERT beyond cancers.

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Non-canonical Telomerase Reverse Transcriptase Controls Osteogenic Reprogramming of Aortic Valve Cells Through STAT5

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Project description:Chemical modifications on mRNA are increasingly recognized as a critical regulatory layer of the flow of genetic information, but quantitative tools to monitor RNA modifications in a whole-transcriptome and site-specific manner are lacking. Here we describe a versatile directed evolution platform that rapidly selects for reverse transcriptases that install mutations during reverse transcription at sites of a given type of RNA modification, allowing for site-specific identification of the modification. To develop and validate the platform, we evolved the HIV-1 reverse transcriptase against N1-methyladenosine (m1A). Iterative rounds of selection yielded reverse transcriptases with both robust read-through and high mutation rates at m1A sites. We apply the evolved reverse transcriptase to identify thousands of statistically confident m1A sites in human mRNA, some of which can be detected in antibody-free RNA-seq libraries. Together, this work develops and validates the reverse transcriptase evolution platform and provides new tools, analysis methods, and datasets to study m1A biology.

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