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Hypoxia regulates endogenous double-stranded RNA production via reduced mitochondrial DNA transcription

ABSTRACT: Hypoxia regulates endogenous double-stranded RNA production via reduced mitochondrial DNA transcription

PROVIDER: PRJNA643232 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12118983_1.fastq.gz	Fastqsanger.gz
	SRR12118983_2.fastq.gz	Fastqsanger.gz
	SRR12118984_1.fastq.gz	Fastqsanger.gz
	SRR12118984_2.fastq.gz	Fastqsanger.gz
	SRR12118985_1.fastq.gz	Fastqsanger.gz

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Hypoxia regulates endogenous double-stranded RNA production via reduced mitochondrial DNA transcription

Project description:Hypoxia is a common phenomenon in solid tumours strongly linked to the hallmarks of cancer. Increasing evidence shows that hypoxia promotes local immune suppression and downregulates the expression of type I interferon (IFN) pathway which is actively involved in current anti-cancer therapies’ success. It was recently described that double-stranded RNA (dsRNA), transiently generated during mitochondrial transcription, endogenously activate the type I IFN pathway. The aims of this study were to determine the effects of hypoxia on the generation of mitochondrial dsRNA (mtdsRNA) in breast cancer, and the mechanisms involved. A significant decrease in dsRNA production was observed in different cell lines under hypoxia in a HIF1/2α-independent manner. dsRNA from mitochondrial fraction was responsible for activation of the type I IFN and significantly decreased after hypoxia treatment. Mitochondrial encoded genes were downregulated in hypoxic samples and in dsRNA-pull-down experiments using the J2 antibody suggesting a reduction in mitochondrial transcription during hypoxia.

2021-06-30 | GSE153557 | GEO

Hypoxia Regulates Endogenous Double-Stranded RNA Production via Reduced Mitochondrial DNA Transcription.

Project description:Hypoxia is a common phenomenon in solid tumours strongly linked to the hallmarks of cancer. Hypoxia promotes local immunosuppression and downregulates type I interferon (IFN) expression and signalling, which contribute to the success of many cancer therapies. Double-stranded RNA (dsRNA), transiently generated during mitochondrial transcription, endogenously activates the type I IFN pathway. We report the effects of hypoxia on the generation of mitochondrial dsRNA (mtdsRNA) in breast cancer. We found a significant decrease in dsRNA production in different cell lines under hypoxia. This effect was HIF1α/2α-independent. mtdsRNA was responsible for induction of type I IFN and significantly decreased after hypoxia. Mitochondrially encoded gene expression was downregulated and mtdsRNA bound by the dsRNA-specific J2 antibody was decreased during hypoxia. These findings reveal a new mechanism of hypoxia-induced immunosuppression that could be targeted by hypoxia-activated therapies.

| S-EPMC8651540 | biostudies-literature

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Project description:To investigate possible smRNAs linked to TMM silencing by single-stranded and double-stranded silencers, we determined sequences of smRNAs by the Illumina high-throughput sequencing platform and compared silencing efficiency of different strategies. We found that single-stranded silencer alone could promote the production of smRNAs.

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In plants, decapping prevents RDR6-dependent production of small interfering RNAs from endogenous mRNAs

Project description:Background: Cytoplasmic degradation of endogenous RNAs is an integral part of RNA quality control (RQC) and often relies on the removal of the 5' cap structure and their subsequent 5M-bM-^@M-^Y to 3M-bM-^@M-^Y degradation. In parallel, many eukaryotes degrade exogenous and selected endogenous RNAs through post-transcriptional gene silencing (PTGS). In plants, PTGS depends on small interfering (si)RNAs produced after the conversion of single-stranded RNAs to double-stranded RNAs by the cellular RNA DEPENDENT RNA POLYMERASE 6 (RDR6). PTGS and RQC compete for transgene-derived RNAs, but it is unknown whether this competition also occurs for endogenous transcripts. Results: We show that that upon decapping impairment hundreds of endogenous mRNAs give rise to a new class of siRNAs, a subset of which depends on RDR6 for their production. Conclusions: Our results suggest that the decapping of aberrant endogenous RNA in P-bodies limits their entry into the PTGS pathway and prevents the subsequent deleterious consequences arising from this entry. We anticipate that the siRNAs identified in decapping mutants represent a subset of a larger ensemble of endogenous siRNAs that we coin rqc-siRNAs because they accumulate when RQC processes are impaired. Small RNA-seq experiments performed in duplicates for each condition.

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