LTR-retrotransposon control by tRNA-derived small RNA
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ABSTRACT:
PROVIDER: PRJNA324286 | ENA |
REPOSITORIES: ENA
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Project description:Transposon reactivation is an inherent danger in cells that lose epigenetic silencing during developmental reprogramming. In the mouse, LTR-retrotransposons, or endogenous retroviruses (ERV), account for most novel insertions and are expressed in the absence of histone H3 Lysine 9 trimethylation in preimplantation stem cells. We found abundant, 18 nt tRNA-derived small RNA (tRF) in these cells, and ubiquitously expressed 22 nt tRFs, that include the 3' terminal CCA of mature tRNAs, and target the tRNA primer binding site (PBS) essential for ERV reverse transcription. We show that the two most active ERV families, IAP and MusD/ETn, are major targets and are strongly inhibited by tRFs in retrotransposition assays. 22 nt tRFs post-transcriptionally silence coding-competent ERVs, while 18 nt tRFs specifically interfere with reverse transcription and retrotransposon mobility. The PBS offers a unique target to specifically inhibit LTR-retrotransposons and tRF-targeting is a potentially highly conserved mechanism of small RNA-mediated transposon control.
2017-06-29 | GSE82199 | GEO
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Project description:Using a TIP-seq protocol (specifically isolating transposon insertion junctions) we determined that the Ty1 retrotransposon targets tRNA genes and, in particular, we determined that the transposon inserts into nucleosomal DNA in an asymmetric pattern. TIP-seq recovery of transposon insertion junctions in haploid and diploid yeast
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Project description:We report polysomal RNA sequencing data (RNAseq), small RNAseq, and virus-like-particle (VLP) DNA sequencing (DNAseq) and ChIPseq data. Arabidopsis ddm1 mutants produce LTR retrotransposon transcripts that are processed into 21-22 nt easiRNAs by RNA-Dependent RNA polymerase 6 (RDR6). To test if 21-22 nt easiRNAs regulate transcription, translation and reverse transcription of LTR retrotransposons, we compared ddm1 and ddm1rdr6 in polysomal RNAseq, VLP DNAseq and ChIPseq data. We found a handful of ATHILA elements were differentially regulated in ddm1rdr6 for polysomal RNAseq, VLP DNAseq, and ChIPseq datasets. Using short read and long read technologies, we also profiled functional LTR retrotransposons that made full-length DNA by reverse transcription inside VLPs. Small RNAseq data were obtained in pollen and inflorescence tissues in wild-type and ddm1.
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Project description:Using a TIP-seq protocol (specifically isolating transposon insertion junctions) we determined that the Ty1 retrotransposon targets tRNA genes and, in particular, we determined that the transposon inserts into nucleosomal DNA in an asymmetric pattern.
2012-01-01 | GSE33986 | GEO
Project description:Long Terminal Repeat (LTR) Retrotransposons are an abundant class of genomic parasites that replicate by insertion of new copies into the host genome. LTR retrotransposons prevent mutagenic insertions through diverse targeting mechanisms that avoid coding sequences, but a universal set of principles guiding their target site selection hasn’t been established. Here we show that insertion of the fission yeast LTR retrotransposon Tf1 is guided by the DNA binding protein Sap1, and that the efficiency and location of the targeting depend on the activity of Sap1 as a replication fork barrier. We propose that Sap1 guides insertion of Tf1 by blocking the progression of the replication fork, and that the Tf1 transposon uses features of arrested forks to insert into the host genome. These observations point to a universal mechanism for determination of LTR retrotransposon target site selection.
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Project description:Long noncoding RNAs transcribed by ERV-9 LTR retrotransposon act in cis to modulate long-range LTR enhancer function
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Project description:LTR retrotransposons are repetitive DNA elements comprising ~10% of the human genome. However, Whether or how the LTR lncRNAs serve biological functions is largely unknown. Here we show that in primary human erythroblasts, lncRNAs transcribed from the LTR retrotransposons of ERV-9 human endogenous retrovirus regulated transcription of key erythroid genes. Global knock-down of ERV-LTR lncRNAs was performed in the in vitro erythropoiesis system of human CD34 cells, and genome wide RNA-seq was carried out to detect the effect on transcription.
2017-01-07 | GSE93280 | 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 | 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