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HIV-1 m6A methylome investigation by m6A-SAC-seq

ABSTRACT: HIV-1 m6A methylome investigation by m6A-SAC-seq

PROVIDER: PRJNA1142507 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30056800_1.fastq.gz	Fastqsanger.gz
	SRR30056800_2.fastq.gz	Fastqsanger.gz
	SRR30056801_1.fastq.gz	Fastqsanger.gz
	SRR30056801_2.fastq.gz	Fastqsanger.gz
	SRR30056802_1.fastq.gz	Fastqsanger.gz

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HIV-1 m6A methylome investigation by m6A-SAC-seq

Project description:Despite effective antiretroviral therapy at reducing HIV-1 viral loads to undetectable levels, the presence of latently infected CD4+ T cells poses a major barrier to HIV-1 cure. N6-methyladenosine (m6A) modification of viral and cellular RNA has a functional role in regulating HIV-1 infection. m6A modification of HIV-1 RNA can affect its stability, translation, and splicing in cells and suppresses type-I interferon induction in macrophages. However, the function of m6A modification in regulating HIV-1 latency reactivation remains unknown. We used the Jurkat T cell line-derived HIV-1 latency model (J-Lat cells) to investigate changes in m6A levels of cellular RNA in response to latency reversal. We observed a significant increase in m6A levels of total cellular RNA upon reactivation of latent HIV-1 in J-Lat cells. This increase in m6A levels was transient and returned to steady-state levels despite continued high levels of viral gene expression in reactivated cells compared to control cells. Upregulation of m6A levels occurred without significant changes in the protein expression of m6A writers or erasers that add or remove m6A, respectively. Knockdown of m6A writers in J-Lat cells significantly reduced HIV-1 reactivation. Treatment of a m6A writer inhibitor reduced cellular RNA m6A levels along with reduction in HIV-1 reactivation. Furthermore, using m6A-specific sequencing, we identified cellular RNAs that are differentially m6A-modified during HIV-1 reactivation in J-Lat cells. Knockdown of identified m6A-modified RNA validate these results with established primary CD4+ T-cell models of HIV-1 latency. These results showed the importance of m6A RNA modification in HIV-1 latency reversal.

2024-10-01 | GSE273614 | GEO

m6A-SAC-seq for quantitative whole transcriptome m6A profiling

Project description:m6A-SAC-seq for quantitative whole transcriptome m6A profiling

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SAC-seq for transcriptome-wide quantitative sequencing of mRNA m6A at base resolution

Project description:Here, we reported transcriptome-wide m6A modification maps within single-base resolution using m6A-SAC-seq in rice and Arabidopsis. Our analysis uncovered a total of 205,691 m6A sites distributed across 22,574 genes in rice, and 188,282 m6A sites across 19,984 genes in Arabidopsis.

2024-04-19 | GSE243722 | GEO

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2024-04-19 | GSE245738 | GEO

m6A sequencing of HIV viral genomic RNA and infected host cell samples

Project description:The internal N6-methyladenosine (m6A) methylation of eukaryotic nuclear RNA controls post-transcriptional gene expression, which is regulated by methyltransferases (writers), demethylases (erasers), and m6A-binding proteins (readers) in cells. The YTH domain family proteins (YTHDF1–3) bind to m6A-modified cellular RNAs and affect RNA metabolism and processing. Here, we show that YTHDF1–3 proteins recognize m6A-modified HIV-1 RNA and inhibit HIV-1 infection in cell lines and primary CD4+ T-cells. We further mapped the YTHDF1–3 binding sites in HIV-1 RNA from infected cells. We found that the overexpression of YTHDF proteins in cells inhibited HIV-1 infection mainly by decreasing HIV-1 reverse transcription, while knockdown of YTHDF1–3 in cells had the opposite effects. Moreover, silencing the m6A writers decreased HIV-1 Gag protein expression in virus-producing cells, while silencing the m6A erasers increased Gag expression. Our findings suggest an important role of m6A modification of HIV-1 RNA in viral infection and HIV-1 protein synthesis.

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Project description:Several prior reports have demonstrated that the epitranscriptomic addition of m6A to viral transcripts promotes the replication and pathogenicity of a wide range of viruses yet the underlying mechanism(s) causing this positive effect has remained unclear. It is known that m6A function is largely mediated by cellular m6A binding proteins or readers, however, how these m6A reader proteins contribute to the regulation of HIV-1 gene expression has remained controversial. Here, we confirm that m6A indeed enhances HIV-1 gene expression. We demonstrate that this effect is collectively mediated by the cytoplasmic reader YTHDF2, which increases HIV-1 transcript stability, and the nuclear m6A reader YTHDC1, which binds HIV-1 RNA at 7 distinct m6A methylated sites, regulating viral transcript alternative splicing.

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Epitranscriptomic addition of m6A regulates HIV-1 RNA stability and alternative splicing

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RNA m6A methylome of Caenorhabditis elegans

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Project description:m6A-Label-seq directly reports m6A methylome at base resolution

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m6A methylome in JQ1 treatment and control in MDA-MB-231 cells.

Project description:We report the application of MeRIP sequencing technology for high-throughput profiling of m6A methylome in breast cancer cells. Comparison of m6A methylome between control and BETi-treated cells revealed the following findings: 1) Significant global alteration of methylation sites due to BETi-treatment (herein defined as BETi-m6A signature). 2) Gene Ontology (GO) analysis of the differential meRIP-seq candidates enriched pathways involved in chromatin modification, RNA splicing and pathways regulating cell fate , reflecting a critical role of m6A in diverse biological processes.

2023-12-31 | GSE219190 | GEO

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