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RNA-RNA interaction analysis of functional SINE repeat elements-derived transcripts

ABSTRACT: RNA-RNA interaction analysis of functional SINE repeat elements-derived transcripts

PROVIDER: PRJNA931610 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23341282.fastq.gz	Fastqsanger.gz
	SRR23341283.fastq.gz	Fastqsanger.gz
	SRR23341284.fastq.gz	Fastqsanger.gz
	SRR23341285.fastq.gz	Fastqsanger.gz

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RNA-RNA interaction analysis of functional SINE repeat elements-derived transcripts

Project description:We studied functional and structural features of mouse and human SINE repeat elements-derived RNAs in SINEUP long non-coding RNAs which upregulate the translation of the target protein coding gene. To check the interaction of functional SINE RNAs with ribosomal RNAs, we created PARIS2 (psoralen analysis of RNA interactions and structures) libraries from SINEUP (with embedded mouse SINEB2 or human FRAM repeat) and the target sense GFP plasmids co-transfected human cells.

2023-02-06 | GSE224533 | GEO

In-cell RNA secondary structure analysis of functional SINE transcripts

Project description:SINEUPs are long non-coding RNAs which contain a functionally crucial SINE repeat element and positively regulate target mRNA translation at post-transcription level. To study secondary (2D) structure of these functional SINE-derived RNAs, various SINEUP-GFP plasmids containing different mouse SINEB2 repeat elements or human SINE FRAM repeat were transfected along with sense EGFP plasmid in HEK293T/17 cells. Total RNA in transfected cells were probed at flexible regions with NAI-N3 reagent and icSHAPE (in-vivo click selective hydroxyl acylation and profiling experiment) libraries were prepared. To further understand the structure dynamics of SINE transcripts in subcellular locations, cells were fractionated in nuclear and cytoplasmic fractions after 24 h of transfection and fraction-specific icSHAPE libraries were constructed.

2023-02-06 | GSE224534 | GEO

In-cell RNA secondary structure analysis of functional SINE transcripts

Project description:In-cell RNA secondary structure analysis of functional SINE transcripts

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SINE RNAs trigger noncanonical NLRC4 inflammasome via DDX17

Project description:Short interspersed element (SINE) RNAs are upregulated by cellular stresses1 (heat shock, DNA damage and viral infection) and accumulate in human diseases (macular degeneration2, lupus3, and Alzheimer’s disease4). These transcripts activate inflammasomes5, a family of cytoplasmic multiprotein complexes that sense danger molecules and initiate innate immune responses by activating caspase-1-dependent cytokine production and inflammatory death6, but the molecular sensor of SINE RNAs is unknown. Here, we identify DDX17, a member of the DEAD box family of RNA helicases7, as a sensor of SINE RNAs requisite for inflammasome activation. Induction of caspase-1 cleavage and release of IL-1 and IL-18 by SINE RNAs requires dual recruitment of NLRP3 and NLRC4 but proceeds independent of NAIPs, immune sensors required for canonical NLRC4 activation by bacterial proteins8,9. Instead, SINE RNAs trigger DDX17–NLRC4 interaction, which licenses inflammasome activation. We also report increased levels of DDX17 protein and association of DDX17 and NLRC4 in the retinal pigmented epithelium (RPE) of human eyes with an advanced, untreatable form of age-related macular degeneration (AMD). Disrupting DDX17–NLRC4 signalling blocks SINE RNA-induced inflammasome activation in human RPE cells and RPE degeneration in an animal model of AMD. Our findings uncover a non-canonical mode of inflammasome activation by endogenous retrotransposon transcripts, and provide new potential targets for macular degeneration and potentially other diseases.

2022-06-09 | PXD016019 | Pride

Next generation sequencing of MA-10 mouse Leydig tumor cells facilitates quantitative analysis of SINE B2-antisense transcripts with the RNAi system: wild type and Dicer1-knockdown transcriptomes

Project description:We report the comparison between SINE B2-AS transcriptome profiling and Dicer1-deficient-cell transcriptome profiling using RNA-seq analysis. We report that thousands of SINE B2 copies encode long B2-AS transcripts, which are constantly degraded by Dicer1. This new class of B2-AS transcripts regulates the expression of SINE B2 sense (B2-S) transcripts. Long B2-S is the main cause of cellular toxicity likely mediated by the multifunctional protein TSPO. Some B2-AS transcripts are putative miRNAs interconnected with the RNAi system. We propose that B2-AS transcripts have evolved as a self-defense mechanism to subvert the host RNAi system.

2020-09-01 | GSE126041 | GEO

Mouse SINE B2 elements function as IFN-inducible enhancer elements [RNA-Seq]

Project description:Mouse SINE B2 elements function as IFN-inducible enhancer elements [RNA-Seq]

| PRJNA836593 | ENA

RNA-seq analysis about Lx8-SINE B2 knocked down samples

Project description:We identified a novel long non-coding RNA Lx8-SINE B2, that is a marker of pluripotency. Depletion of Lx8-SINE B2 impacts embryonic stem cell self-renewal. RNA-seq analysis of Lx8-SINE B2 depletion revealed that a number of glycolytic genes with decreased expression. Mechanistically, we found that the Lx8-SINE B2 activates the glycolysis pathway by binding to Eno1. Collectively, our data suggest that Lx8-SINE B2 maintains the self-renewal of mESCs through glycolysis.

2022-09-19 | GSE182247 | GEO

B2 SINE expression during MHV68 infecton

Project description:Short interspersed nuclear elements (SINEs) are retrotransposons evolutionarily derived from endogenous RNA Polymerase III RNAs. Though SINE elements have undergone exaptation into gene regulatory elements, how transcribed SINE RNA impacts transcriptional and post-transcriptional regulation is largely unknown. This is partly due to a lack of information regarding which of the loci have transcriptional potential. Here, we present an approach (short interspersed nuclear element sequencing, SINE-seq), which selectively profiles RNA Polymerase III-derived SINE RNA, thereby identifying transcriptionally active SINE loci. Applying SINE-seq to monitor murine B2 SINE expression during a gammaherpesvirus infection revealed transcription from 28,270 SINE loci, with ~50% of active SINE elements residing within annotated RNA Polymerase II loci. Furthermore, B2 RNA can form intermolecular RNA-RNA interactions with complementary mRNAs, leading to nuclear retention of the targeted mRNA via a mechanism involving p54nrb. These findings illuminate a pathway for the selective regulation of mRNA export during stress via retrotransposon activation.

2016-10-31 | GSE85518 | GEO

m6A RNA methylation of major satellite repeat transcripts facilitates chromatin association and RNA:DNA hybrid formation in mouse heterochromatin

Project description:m6A RNA methylation of major satellite repeat transcripts facilitates chromatin association and RNA:DNA hybrid formation in mouse heterochromatin

2021-04-21 | GSE156481 | GEO

Phenylalanine-tRNA aminoacylation is compromised by ALS/FTD-associated C9orf72 C4G2 repeat RNA

Project description:The expanded hexanucleotide GGGGCC repeat mutation in the C9orf72 gene is the main genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia. Under one disease mechanism, sense and antisense transcripts of the repeat are predicted to bind various RNA-binding proteins, compromise their function and cause cytotoxicity. Focusing on cytoplasmic interaction of the CCCCGG antisense repeat RNA this study identifies phenylalanine-tRNA synthetase (FARS) subunit alpha (FARSA) as the main interactor. The aminoacylation of tRNAPhe by FARS is inhibited by antisense RNA, leading to decreased levels of charged tRNAPhe. Remarkably, this is associated with global reduction of phenylalanine incorporation in the proteome and significant decrease in expression of phenylalanine-rich proteins in cellular models and patient tissues. In conclusion, this research reveals functional inhibition of FARSA in the presence of antisense RNA repeats. Compromised aminoacylation of tRNA could lead to impairments in protein synthesis and further contribute to C9orf72 mutation-associated pathology.

2023-09-18 | PXD042474 | Pride

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