TsRNA epitranscriptomics
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB57983 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR10557905.fastq.gz | Fastqsanger.gz | |||
| ERR10557906.fastq.gz | Fastqsanger.gz | |||
| ERR10557907.fastq.gz | Fastqsanger.gz | |||
| ERR10557908.fastq.gz | Fastqsanger.gz | |||
| ERR10557909.fastq.gz | Fastqsanger.gz |
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Project description:Transfer RNA (tRNA) molecules contain a variety of post-transcriptional modifications which are crucial for tRNA stability, translation efficiency, and fidelity. Besides their canonical roles in translation, tRNAs also originate tRNA-derived small RNAs (tsRNAs), a class of small non-coding RNAs with regulatory functions ranging from translation regulation, to gene expression control and cellular stress response. Recent evidence show that tsRNAs are also modified, however the impact of tRNA epitranscriptome deregulation on tsRNAs generation is only now beginning to be uncovered. The 5-methyluridine (m5U) modification at position 54 of cytosolic tRNAs is one of the most common and conserved tRNA modifications among species. This modification is catalyzed by the tRNA methyltransferase TRMT2A, but its biological role remains largely unexplored. Here, we show that TRMT2A knockdown in human cells induces m5U54 tRNA hypomodification, resulting in angiogenin (ANG) dependent tsRNA formation. More specifically, m5U54 hypomodification is followed by ANG overexpression and tRNA cleavage near the anticodon, resulting in accumulation of 5’tRNA-derived stress-induced RNAs (5’tiRNAs), in particular 5’tiRNA-GlyGCC and 5’tiRNA-GluCTC. Additionally, transcriptomic analysis confirms that down-regulation of TRMT2A and consequently m5U54 hypomodification impacts the cellular stress response and RNA stability, which is often correlated with tsRNA generation. Accordingly, exposure to oxidative stress conditions induces TRMT2A down-regulation and tsRNA formation in mammalian cells. These results establish a link between tRNA demethylation and tsRNAs formation and unravel m5U54 as a tRNA cleavage protective mark.
2021-04-20 | GSE164168 | GEO
Project description:Transfer RNA (tRNA) molecules contain a variety of post-transcriptional modifications which are crucial for tRNA stability, translation efficiency, and fidelity. Besides their canonical roles in translation, tRNAs also originate tRNA-derived small RNAs (tsRNAs), a class of small non-coding RNAs with regulatory functions ranging from translation regulation, to gene expression control and cellular stress response. Recent evidence show that tsRNAs are also modified, however the impact of tRNA epitranscriptome deregulation on tsRNAs generation is only now beginning to be uncovered. The 5-methyluridine (m5U) modification at position 54 of cytosolic tRNAs is one of the most common and conserved tRNA modifications among species. This modification is catalyzed by the tRNA methyltransferase TRMT2A, but its biological role remains largely unexplored. Here, we show that TRMT2A knockdown in human cells induces m5U54 tRNA hypomodification, resulting in angiogenin (ANG) dependent tsRNA formation. More specifically, m5U54 hypomodification is followed by ANG overexpression and tRNA cleavage near the anticodon, resulting in accumulation of 5’tRNA-derived stress-induced RNAs (5’tiRNAs), in particular 5’tiRNA-GlyGCC and 5’tiRNA-GluCTC. Additionally, transcriptomic analysis confirms that down-regulation of TRMT2A and consequently m5U54 hypomodification impacts the cellular stress response and RNA stability, which is often correlated with tsRNA generation. Accordingly, exposure to oxidative stress conditions induces TRMT2A down-regulation and tsRNA formation in mammalian cells. These results establish a link between tRNA demethylation and tsRNAs formation and unravel m5U54 as a tRNA cleavage protective mark.
2021-04-20 | GSE164405 | GEO
Project description:The expression levels of tRNA-derived small RNA, known as tsRNA, were interrogated in the following parental cell lines: MCF10A normal-like mammary epithelial cell, MCF7, MCF10AT1, MCF10CA1a, and MDA-MB-231 breast cancer cells. In addition, tsRNA expression was determined after shRNA-inhibition of RUNX1 in MCF10A cells or RUNX1 induction in MCF10CA1a cells.
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Project description:Emerging evidence indicates that tRNA-derived small RNAs (tsRNAs) with the most abundant RNA modifications play an important role in many complex physiological and pathological processes. However, the biological function and regulation mechanism of modified tsRNA in cancer are still poorly understood. Here, we screened and confirmed a novel m7G modified tsRNA, m7G-3'tiRNA LysTTT (mtiRL) in a variety of chemical carcinogenic models by combined small RNA sequencing with m7G small RNA modified Chip. Moreover, we found that mtiRL catalyzed by tRNA m7G modifying enzyme mettl1 promoted bladder cancer malignancy in vitro and in vivo. Mechanistically, mtiRL specifically bound to oncoprotein Annexin A2 (ANXA2) to promote Tyr24 phosphorylation of ANXA2 by enhancing interactions between ANXA2 and YES1, leading to ANXA2 activation and increased ANXA2 nuclear distribution in bladder cancer cells. Together, these findings define a critical role for mtiRL, targeting this novel m7G modified tsRNA would be an efficient way for the treatment of BC.
2024-05-11 | GSE232579 | GEO
Project description:To identify tRNA fragments regulated by angiogenin (ANG, Rnase 5), we sequenced 15-50nt small RNAs upon ANG overexpression and ANG knockout.
2019-10-01 | GSE130764 | GEO
Project description:tsRNA is newly found small non-coding RNA with important biological function. However, the knowlede of diversity, biogeneis and function of tsRNA in plant is still lacking. Here, we selected 10-60 nt small RNA for high-throughput sequencing and uncovered the diversity,biogenesis and potentical function of tsRNA in Arabidopsis.
2021-03-07 | GSE95768 | GEO
Project description:We report the identification and quantification of Watson-Crick modifications in tRNA and rRNA through the use of high throughput sequencing. We apply the recently published DM-tRNA-Seq method to generate demethylase treated and untreated 293T samples, and using computational methods we are able to flag sites using a modification index. This index allows us to generate site-resolved information about modification that we can use to identify and quantify Watson-Crick face modifications in tRNA and rRNA. With the demethylase treated samples, we are able to validate numerous nucleotide modifications from demethylase substrates, and the absence of demethylase action also serves to aid in identification. We find numerous novel modification sites in tRNA as well as striking comparisons between tissues cultures lines. Our study reports a comprehensive analysis of the tRNA modification landscape by identifying sites of modification as well as quantifying modification levels.
2017-02-10 | GSE76434 | GEO
Project description:Age is an independent risk factor for atrial fibrillation (AF), and curcumin can delay aging related disease through reducing oxidative stress and inflammation. However, its target in aging-related AF remains unclear. Transfer RNA-derived small RNA (tsRNA) is a novel short non-coding RNA (sncRNA), and exerts a potential regulatory function in aging. This study was to explore the therapeutic targets of curcumin in atrium of aged mice by PANDORA-seq. Aged mice (18 month) were treated with curcumin (100mg/kg). Rapid transjugular atrial pacing was performed to observe AF inducibility. SA-β-gal staining, ROS detection and qRT-PCR were used to assess the degree of aging and oxidative stress/inflammation levels. PANDORA-seq was performed to reveal the differentially expressed sncRNAs in the atrium of mice. The results showed that curcumin reduced the susceptibility AF of aged mice by improving aging-related atrial fibrosis. Compared to young mice (5 month) group, aged mice yielded 473 significantly altered tsRNA sequences, while 947 tsRNA sequences were significantly altered after treated with curcumin. Enrichment analysis revealed that the target genes were mainly related to DNA damage and protein modification. Compared with the 5mo group, the expression levels of mature-mt_tRNA-Val-TAC_CCA_end, mature-mt_tRNA-Glu-TTC_CCA_end, and mature-tRNA-Asp-GTC_CCA_end were up-regulated in the 18mo group, while the expression of mature-mt_tRNA-Thr-TGT_5_end was down-regulated. This trend was reversed in the 18mo+curcumin group. Increased cellular ROS levels, inflammation expression and senescence in aged mice atrium were improved by the down-regulation of mature-mt_tRNA-Val-TAC_CCA_end. In conclusion, our findings identified mature-mt_tRNA-Val-TAC_CCA_end participated in the mechanism of aging-related atrial fibrosis, providing new intervention target of aging-related AF.
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Project description:To identify and characterize differentially expressed tsRNA, we collected 3 primary tissues and 3 liver metastasis tissues in pancreatic cancer, and compared the tsRNA expression profiles between primary tissues and liver metastasis tissues in pancreatic cancer using tsRNA sequencing.
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Project description:Chronic obstructive pulmonary disease (COPD) is characterized by lung parenchymal destruction and small airway remodeling, involving processes like inflammation, cell apoptosis, epithelial-mesenchymal transition (EMT), and collagen deposition. There are currently no targeted drugs for airway remodeling. Bone marrow mesenchymal stem cells (BMSCs) show promise in COPD treatment, yet their impact on airway remodeling and underlying mechanisms remain elusive. Transfer RNA-derived small RNAs (tsRNAs) are non-coding RNAs implicated in disease regulation, but their role in COPD and their modulation by BMSCs remain unexplored. Our study assessed BMSC effects on airway remodeling in a COPD mouse model and constructed tsRNA and mRNA expression profiles. Based on the differentially expressed tsRNA-mRNA target pairs identified by tsRNA and mRNA sequencing, we constructed a tsRNA regulatory network linked to COPD airway remoding. The modulation of tsRNA by MSCs may represent one of the pathways through which they ameliorate COPD airway remodeling. Our research will enrich the understanding of BMSC therapy for COPD and provide greater insight into the molecular mechanisms underlying the progression and treatment of airway remodeling.
2024-12-05 | GSE262564 | GEO