M6A modification of EBV transcripts
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA530545 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8836880.fastq.gz | Fastqsanger.gz | |||
| SRR8836890.fastq.gz | Fastqsanger.gz | |||
| SRR8836881.fastq.gz | Fastqsanger.gz | |||
| SRR8836891.fastq.gz | Fastqsanger.gz | |||
| SRR8836882.fastq.gz | Fastqsanger.gz |
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Project description:We examined the viral epitranscriptome in EBV transformed lymphoblastoid cell lines (LcLs) and EBV-positive Burkitt's lymphoma, Akata cells, using methylated RNA immunoprecipitation followed by sequencing (MeRIP-seq). Biological replicates of ribo-RNA deleted mRNA of each cell type were prepared for MeRIP-seq followed by peak calling using the exome Peak package with settings for stringent peak calling on both strands of the genome.
2023-08-12 | GSE129217 | GEO
Project description:Purpose: Evaluation of the m6A modification of EBV and BJAB transcripts during EBV infection Methods: Human B lymphoma cell line BJAB was uninfected or infected with EBV for 24 hours. Total RNA from each sample were extracted. Intact mRNA was isolated from total RNA samples and then chemically fragmented to 100-nucleoside-long fragments. m6A methylated mRNAs were immunoprecipitated with anti-N6-methyadenosine (m6A) antibody (a part of the fragmented mRNAs was kept as input). Both m6A enriched mRNAs and input mRNAs were concentrated for RNA-seq library construction. Sequencing was performed using an Illumina HiSeq 4000. Results: EBV EBNA2 and BHRF1 transcripts were m6A modified and m6A modification of BJAB transcripts changed during EBV infection. Conclusions: Our study found that some EBV transcripts were m6A modified during EBV infection and EBV infection changed m6A modification profiles of BJAB transcripts.
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Project description:N6-methyladenosine (m6A) modification is one of the most abundant post-transcriptional modifications that plays an important role in many pathophysiological conditions including host-pathogen interactions. A number of viruses were previously shown to manipulate the cellular m6A machinery usurping its function to their benefit during the course of their life cycle. Previously, we reported that EBV reprograms the host m6A system to regulate the stability of the viral transcripts and drive viral-mediated tumorigenesis by hijacking the functions of methyltransferase METTL14. We now report that during lytic reactivation EBV targets the RNA methylation system of the host to attenuate the innate immune response by suppressing the interferon response to facilitate a successful lytic replication.
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Project description:The RNA modification N6-methyladenosine (m6A) can modulate mRNA fate and thus affect many biological processes. We analyzed m6A modification across the transcriptome following infection by dengue virus (DENV), Zika virus (ZIKV), West Nile virus (WNV), and hepatitis C virus (HCV). We found that infection by these viruses in the Flaviviridae family alters m6A modification of specific cellular transcripts, including RIOK3 and CIRBP. During viral infection, the addition of m6A to RIOK3 promotes its translation, while loss of m6A in CIRBP promotes alternative splicing. Importantly, we found that viral activation of innate immune sensing or the endoplasmic reticulum (ER) stress response contributes to the changes in m6A modification in RIOK3 and CIRBP, respectively. Further, several transcripts with infection-altered m6A profiles, including RIOK3 and CIRBP, encode proteins that influence DENV, ZIKV, and HCV infection. Overall, this work reveals that cellular signaling pathways activated during viral infection lead to alterations in m6A modification of host mRNAs to regulate infection.
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Project description:N6-methyl-adenosine (m6A) is the most abundant modification on messenger RNAs and is linked to human diseases, but its functions in mammalian development are poorly understood. Here we reveal the evolutionary conservation and function of m6A by mapping the m6A methylome in mouse and human embryonic stem cells. Thousands of messenger and long noncoding RNAs show conserved m6A modification, including transcripts encoding core pluripotency transcription factors. m6A is enriched over 3M-bM-^@M-^Y untranslated regions at defined sequence motifs, and marks unstable transcripts, including transcripts turned over upon differentiation. Genetic inactivation or depletion of mouse and human Mettl3, one of the m6A methylases, led to m6A erasure on select target genes, prolonged Nanog expression upon differentiation, and impaired ESCM-bM-^@M-^Ys exit from self-renewal towards differentiation into several lineages in vitro and in vivo. Thus, m6A is a mark of transcriptome flexibility required for stem cells to differentiate to specific lineages. Examing m6A modification differences in two different cell types
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Project description:Altered m6A Modification of Specific Cellular Transcripts Affects Flaviviridae Infection
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Project description:Our study demonstrated that the expression of Igf2bp1 in activated microglia was significantly up-regulated, implying a role of Igf2bp1 in LPS-induced m6A modifications in microglia. To understand the roles of Igf2bp1 on LPS-induced m6A modification in microglia, we performed Igf2bp1 loss-of-function (LOF) approach. Microglia stimulated by LPS were transfected with either scrambled siRNA control or Igf2bp1 siRNA for 48 hours. To m6A modification profiles in control and Igf2bp1 LOF microglia were determined by MeRIP-seq analysis.
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Project description:N6-methyladenosine (m6A) is a widespread reversible chemical modification of RNAs, implicated in many aspects of RNA metabolism. Little quantitative information exists as to either how many transcript copies of particular genes are m6A modified (âm6A levelsâ), or the relationship of m6A modification(s) to alternative RNA isoforms. To deconvolute the m6A epitranscriptome, we developed m6A level and isoform-characterization sequencing (m6A-LAIC-seq). We found that cells exhibit a broad range of non-stoichiometric m6A levels with cell type specificity. At the level of isoform characterization, we discovered widespread differences in use of tandem alternative polyadenylation (APA) sites by methylated and nonmethylated transcript isoforms of individual genes. Strikingly, there is a strong bias for methylated transcripts to be coupled with proximal APA sites, resulting in shortened 3â untranslated regions (3â-UTRs), while nonmethylated transcript isoforms tend to use distal APA sites. m6A-LAIC-seq yields a new perspective on transcriptome complexity and links APA usage to m6A modifications. m6A-LAIC-seq of H1-ESC and GM12878 cell lines, each cell line has two replicates
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Project description:Here we determine the map of RNA methylation (m6A) in mouse embrionic stem cells, and Mettl3 knock out cells Examination of m6A modification sites on the transcriptome of mouse Embryonic stem cells and Embryonic Mettl3 knock out cells, using a m6A specific antibody.
2014-10-16 | E-GEOD-52662 | biostudies-arrayexpress
Project description:We report the application of specific antibodies and high-throughput sequencing technologies (methylated RNA immunoprecipitation sequencing, MeRIP-seq) for high-throughput profiling of m6A modifications in NSCLC cisplatin resistant cells. We generated maps of m6A modified transcripts in A549 and A549/DDP cells. We find that the m6A level was significantly increased in A549/DDP cells compared to the A549 cells. We show that there was a close correlation between the m6A modification and cisplatin resistance.
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