HIV-1 m6A methylome investigation by m6A-SAC-seq [CD4+ T cells]
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PROVIDER: PRJNA1179418 | ENA |
REPOSITORIES: ENA
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Project description:HIV-1 m6A methylome investigation by m6A-SAC-seq
| PRJNA1142507 | ENA
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
Project description:N6-methyladenosine (m6A) is the most prevalent cellular mRNA modification and plays an important role in RNA stability, localization, and gene expression. There are several papers reported that HIV-1 infection upregulates cellular RNA m6A in CD4+ T cells, and this upregulation occurs without changes to the expression levels of the cellular enzymes which add or remove m6A. However, the mechanism of HIV-1 inducing cellular mRNA m6A upregulation is unknown. Here we show that HIV-1 infection upregulates m6A of cellular mRNA and promotes METTL3/METTL14 interaction. We found that HIV-1 infection resulted in increased cellular mRNA m6A level in activated primary CD4+ T cells detected by m6A dot blot and m6A ELISA. We found that HIV-1 infection of CD4+ T cells promotes METTL3/METTL14 interaction compared to mock control using co-immunoprecipitation (co-IP). Our ongoing studies will determine the transcriptomic, epitranscriptomic, and proteomic profiles of CD4+ T cells infected with HIV-1 for 4 days. These studies will facilitate the elucidation of the mechanisms by which HIV-1 infection leads to increased levels of cellular m6A and methyltransferase writers comlex.
2025-05-01 | GSE280563 | GEO
Project description:m6A-SAC-seq for quantitative whole transcriptome m6A profiling
| PRJNA814275 | ENA
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
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 | GSE245738 | GEO
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.
2016-08-18 | GSE85724 | GEO
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.
2021-02-06 | GSE166237 | GEO
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.
2021-06-21 | GSE165473 | GEO
Project description:RNA m6A methylome of Caenorhabditis elegans
| PRJNA625719 | ENA