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RNA Interference01:23

RNA Interference

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RNA interference (RNAi) is a process in which a small non-coding RNA molecule blocks the post-transcriptional expression of a gene by binding to its messenger RNA (mRNA) and preventing the protein from being translated.
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RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing its transcription or activating the RNA degradation process. The mechanism was discovered by Andrew Fire and Craig Mello in 1998 in plants. Today, it is observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals. This precise cellular mechanism of gene silencing has been developed into a technique that provides an efficient way to identify and determine the...
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Small interfering RNAs, or siRNAs, are short regulatory RNA molecules that can silence genes post-transcriptionally, as well as the transcriptional level in some cases. siRNAs are important for protecting cells against viral infections and silencing transposable genetic elements.
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During most eukaryotic translation processes, the small 40S ribosome subunit scans an mRNA from its 5' end until it encounters the first start AUG codon. The large 60S ribosomal subunit then joins the smaller one to initiate protein synthesis. The location of the translation initiation is largely determined by the nucleotides near the start codon as there may be multiple translation initiation sites present on the mRNA.  Marilyn Kozak discovered that the sequence RCCAUGG (where R...
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MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
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RNA viruses are categorized into positive-strand, negative-strand, or double-stranded groups based on their genomic structure and replication mechanisms. This classification dictates how they exploit host cellular machinery for protein synthesis and replication. Some RNA viruses also utilize reverse transcription as part of their life cycle, further diversifying their replication strategies.Positive-Strand RNA VirusesPositive-strand RNA viruses have genomes that function directly as messenger...
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Exploring m6A and m5C Epitranscriptomes upon Viral Infection: an Example with HIV
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Targeting the m6A RNA modification pathway blocks SARS-CoV-2 and HCoV-OC43 replication.

Hannah M Burgess1, Daniel P Depledge2, Letitia Thompson1

  • 1Department of Microbiology, New York University School of Medicine, New York, New York 10016, USA.

Genes & Development
|June 25, 2021
PubMed
Summary

The study shows that targeting the N-methyladenosine (m6A) RNA modification pathway can suppress SARS-CoV-2 and HCoV-OC43 replication. Inhibiting METTL3 or m6A readers reduces viral RNA and protein synthesis, offering therapeutic potential.

Keywords:
HCoV-OC43N6-methyladenosineRNA modificationSARS-CoV-2coronavirusdirect RNA sequencingnanopore sequencingvirus–host interactions

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Area of Science:

  • Virology
  • Molecular Biology
  • Epigenetics

Background:

  • N-methyladenosine (m6A) is a key RNA modification affecting RNA fate.
  • The role of m6A machinery in cytoplasmic RNA virus replication, like coronaviruses, is largely unknown.
  • SARS-CoV-2 and other coronaviruses replicate exclusively in the cytoplasm.

Purpose of the Study:

  • To investigate the impact of the cellular m6A modification machinery on coronavirus replication.
  • To determine if targeting m6A pathway components can suppress SARS-CoV-2 and HCoV-OC43 replication.
  • To explore the therapeutic potential of targeting the m6A pathway against coronaviruses.

Main Methods:

  • Depletion of METTL3 and m6A reader proteins (YTHDF1, YTHDF3).
  • Treatment with a specific small molecule METTL3 inhibitor.
  • Methylated RNA immunoprecipitation sequencing (meRIP-seq) to map m6A sites.
  • Quantification of viral RNA and nucleocapsid (N) protein synthesis.

Main Results:

  • Depletion of METTL3 or m6A readers, and METTL3 inhibition, suppressed SARS-CoV-2 and HCoV-OC43 replication.
  • Reduced viral RNA and nucleocapsid (N) protein synthesis correlated with suppressed infectious titer.
  • meRIP-seq identified m6A modification sites on viral RNAs.
  • HCoV-OC43 infection increased nuclear localization of METTL3 and cytoplasmic YTHDF1/YTHDF2.

Conclusions:

  • Coronavirus RNAs are targets of m6A modification.
  • Host m6A pathway components play a crucial role in regulating β-coronavirus replication.
  • Targeting the m6A pathway presents a potential therapeutic strategy to inhibit coronavirus reproduction.