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Induction of a transcriptional adaptation response by RNA destabilization events [dst278]

ABSTRACT: Induction of a transcriptional adaptation response by RNA destabilization events [dst278]

PROVIDER: PRJNA1186596 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31362072_1.fastq.gz	Fastqsanger.gz
	SRR31362072_2.fastq.gz	Fastqsanger.gz
	SRR31362073_1.fastq.gz	Fastqsanger.gz
	SRR31362073_2.fastq.gz	Fastqsanger.gz
	SRR31362074_1.fastq.gz	Fastqsanger.gz

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Induction of a transcriptional adaptation response by RNA destabilization events [dst175]

Project description:Induction of a transcriptional adaptation response by RNA destabilization events [dst175]

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Induction of a transcriptional adaptation response by RNA destabilization events [dst278]

Project description:Transcriptional adaptation (TA) is a cellular process whereby mRNA-destabilizing mutations lead to the transcriptional upregulation of so-called adapting genes. The nature of the TA-triggering factor(s) remains unclear, namely whether an mRNA-borne premature termination codon (PTC) or the subsequent mRNA degradation process, and/or its products, elicits TA. Here, we first established two perturbations leading to mRNA destabilization for mouse Actg1: a Cas9-induced mutation that leads to a PTC, and Cas13d-mediated mRNA cleavage. We find that both perturbations are effective in degrading Actg1 mRNA and upregulating Actg2. Notably, increased chromatin accessibility at the Actg2 locus was observed only in the Cas9-induced mutant allele but not in the Cas13d-targeted cells, suggesting that chromatin remodeling is not required for Actg2 upregulation. We further show that ribozyme-mediated Actg1 pre-mRNA cleavage also leads to a robust upregulation of Actg2. Together, these data highlight the critical role of RNA destabilization events as a trigger for TA.

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Project description:Transcriptional adaptation (TA) is a cellular process whereby mRNA-destabilizing mutations lead to the transcriptional upregulation of so-called adapting genes. The nature of the TA-triggering factor(s) remains unclear. Here, we first generated Cas9-induced mutations in mouse Actg1, including an mRNA-destabilizing allele and an RNA-less allele. We find in the Actg1 mRNA-destabilizing allele, higher levels of Actg2 mRNA as well as increased chromatin accessibility at the Actg2 locus compared with wild-type and the RNA-less allele. Notably, Cas13d experiments show that Actg1 mRNA cleavage, but not Actg1 pre-mRNA cleavage, also triggers Actg2 upregulation; however, this upregulation is not associated with increased chromatin accessibility at the Actg2 locus. Furthermore, time course experiments show that increased Actg2 expression persists even after Actg1 mRNA degradation by Cas13d ceases. Together, our data highlight the importance of cytoplasmic mRNA degradation as a trigger for the TA response and suggest that chromatin remodeling is not necessary for TA.

2025-03-17 | GSE286097 | GEO

Induction of a transcriptional adaptation response by RNA destabilization events

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Induction of a transcriptional adaptation response via perturbations at the DNA and RNA levels

Project description:Induction of a transcriptional adaptation response via perturbations at the DNA and RNA levels

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Functional RNA dynamics are progressively governed by RNA destabilization during the adaptation to chronic hypoxia

Project description:Previous studies towards reduced oxygen availability mostly focused on changes in total mRNA expression neglecting underlying transcriptional and post-transcriptional events. Therefore, we generated a comprehensive overview of hypoxia-induced changes in total mRNA expression, global de novo transcription, and mRNA stability in monocytic THP-1 cells. Since hypoxic epi-sodes often persist for prolonged periods, we further compared adaptations to acute and chronic hypoxia. While total mRNA changes correlated well with enhanced transcription during short term hypoxia, mRNA destabilization gained importance under chronic conditions. Reduced mRNA stability not only added to compensatory attenuation of immune responses, but most no-tably to the reduction of nuclear-encoded mRNAs associated with various mitochondrial func-tions. These changes may prevent the futile production of new mitochondria under conditions where mitochondria cannot exert their full metabolic function and are indeed actively removed by mitophagy. The post-transcriptional mode of regulation might further allow for rapid recov-ery of mitochondrial capacities upon reoxygenation. Our results provide a comprehensive re-source of functional mRNA expression dynamics and underlying transcriptional and post-transcriptional regulatory principles during the adaptation to hypoxia. Furthermore, we specifically uncover mitochondrial functions controlled by RNA stability regulation in the con-text of hypoxia.

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Project description:Induction of a transcriptional adaptation response via perturbations at the DNA and RNA levels [dst233]

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Functional RNA dynamics are progressively governed by RNA destabilization during the adaptation to chronic hypoxia

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