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N6-Methyladenosine Modification of Hepatitis B Virus RNA Differentially Regulates The Viral Life Cycle

ABSTRACT: N6-Methyladenosine Modification of Hepatitis B Virus RNA Differentially Regulates The Viral Life Cycle

PROVIDER: PRJNA471523 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7167361.fastq.gz	Fastqsanger.gz
	SRR7167362.fastq.gz	Fastqsanger.gz
	SRR7167363.fastq.gz	Fastqsanger.gz
	SRR7167364.fastq.gz	Fastqsanger.gz
	SRR7167365.fastq.gz	Fastqsanger.gz

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Similar Datasets

N6-Methyladenosine Modification of Hepatitis B Virus RNA Differentially Regulates The Viral Life Cycle

Project description:N6-methyladenosine (m6A) RNA methylation is the most abundant epitranscriptomic modification of eukaryotic messenger RNAs (mRNAs). Previous reports have found m6A on both cellular and viral transcripts and defined its role in regulating numerous biological processes, including viral infection. Here, we show that m6A and its associated machinery regulate the life cycle of hepatitis B virus (HBV). HBV is a DNA virus that completes its life cycle via an RNA intermediate, termed pregenomic RNA (pgRNA). Silencing of enzymes that catalyze the addition of m6A to RNA resulted in increased HBV protein expression, but overall reduced reverse transcription of the pgRNA. We mapped the m6A site in the HBV RNA and found that a conserved m6A consensus motif situated within epsilon (stem loop structure is the site for m6A modification. The epsilon stem loop is located in the 3’ terminus of all HBV mRNAs and both termini (5’ and 3’) of the pgRNA. Mutational analysis of the identified m6A site in the 5’ epsilon stem loop of pgRNA revealed that m6A at this site is required for efficient reverse transcription of pgRNA, while m6A of the 3’ epsilon stem loop results in destabilization of all HBV transcripts, suggesting that m6A has dual regulatory functions in pgRNA. Overall, this study reveals how m6A regulates HBV gene expression and reverse transcription, leading to a new level of understanding of the HBV life cycle. .

2019-01-01 | GSE114486 | GEO

<i>N6</i>-methyladenosine modification of hepatitis B virus RNA differentially regulates the viral life cycle.

Project description:N6-methyladenosine (m6A) RNA methylation is the most abundant epitranscriptomic modification of eukaryotic messenger RNAs (mRNAs). Previous reports have found m6A on both cellular and viral transcripts and defined its role in regulating numerous biological processes, including viral infection. Here, we show that m6A and its associated machinery regulate the life cycle of hepatitis B virus (HBV). HBV is a DNA virus that completes its life cycle via an RNA intermediate, termed pregenomic RNA (pgRNA). Silencing of enzymes that catalyze the addition of m6A to RNA resulted in increased HBV protein expression, but overall reduced reverse transcription of the pgRNA. We mapped the m6A site in the HBV RNA and found that a conserved m6A consensus motif situated within the epsilon stem loop structure, is the site for m6A modification. The epsilon stem loop is located in the 3' terminus of all HBV mRNAs and at both the 5' and 3' termini of the pgRNA. Mutational analysis of the identified m6A site in the 5' epsilon stem loop of pgRNA revealed that m6A at this site is required for efficient reverse transcription of pgRNA, while m6A methylation of the 3' epsilon stem loop results in destabilization of all HBV transcripts, suggesting that m6A has dual regulatory function for HBV RNA. Overall, this study reveals molecular insights into how m6A regulates HBV gene expression and reverse transcription, leading to an increased level of understanding of the HBV life cycle.

| S-EPMC6126736 | biostudies-literature

Viral and Cellular N6-methyladenosine (m6A) Epitranscriptomes in KSHV Life Cycle

Project description:Tan et al. discovered abundant conserved N6-methyladenosine (m6A) modifications on KSHV transcripts during latent and productive infection in different cell types. They also show that m6A readers YTHDF2 and YTHDF3 mediate KSHV replication, and KSHV optimizes both phases of viral replication by reprograming cellular epitranscriptome to regulate distinct signaling pathways.

2017-10-31 | GSE93676 | GEO

N6-Methyladenosine Modification Controls Circular RNA Immunity.

Project description:N6-Methyladenosine Modification Controls Circular RNA Immunity.

| PRJNA476784 | ENA

N6-methyladenosine (m6A) modification in HEK (primary human epidermal keratinocytes)

Project description:We conducted an analysis of N6-methyladenosine (m6A) modifications in HEK (primary human epidermal keratinocytes). The primary aim of this investigation was to establish a molecular framework elucidating the role of m6A modifications in modulating the functional of keratinocytes.

2024-08-20 | GSE269500 | GEO

Viral and Cellular N6-methyladenosine (m6A) Epitranscriptomes in KSHV Life Cycle

Project description:Viral and Cellular N6-methyladenosine (m6A) Epitranscriptomes in KSHV Life Cycle

| PRJNA361517 | ENA

Landscape of N6-methyladenosine modification patterns in human ameloblastoma

Project description:N6-methyladenosine (m6A) is one of the most popular RNA modifications, which is widely found in messenger RNAs (mRNAs) and non-coding RNA like long no-coding RNA (lncRNAs) and circular RNA (circRNAs).In our study,we provide m6A landscape of human ameloblastoma, which expands the understanding of m6A modifications and uncovers regulation of lncRNAs and circRNAs through m6A modification in ameloblastoma.

2020-10-08 | GSE156886 | GEO

N6-Methyladenosine methylation profile in rat H9C2 cardiomyocytes under the hypoxic stress

Project description:Hypoxia as a crucial pathogenesis factor usually results in huge harmful effects on cardiac injury and dysfunction. In our previous study (PMID: 33294289), We observe a series of differential expressed genes between transcription and translation, which may be attributed to the hypoxia-specific binding affinity of Nuclear cap-binding subunit 3 (NCBP3) at 5’ un-translation region of target genes. But the underlying molecular mechanism of NCBP3 for gene translation modulation remains unclear. Here, we conducted RIP-seq of N6-Methyladenosine methylation in H9C2 cells with the conditions of normoxic, hypoxic and with additional NCBP3 knockdown.

2021-06-30 | E-MTAB-10682 | biostudies-arrayexpress

Landscape of N6-methyladenosine modification patterns in invasive malignant pleomorphic adenoma

Project description:N6-methyladenosine (m6A) is one of the most popular RNA modifications, which is widely found in messenger RNAs (mRNAs) .In our study,we provide m6A profiles of human invasive malignant pleomorphic adenoma, which open an avenue for in-depth knowledge and understanding of m6A topology in invasive malignant pleomorphic adenoma.

2021-03-10 | GSE161879 | GEO

N6-methyladenosine Modulates Messenger RNA Translation Efficiency

Project description:N6-methyladenosine (m6A) is the most abundant internal messenger (mRNA) modification in mammalian mRNA. This modification is reversible and non-stoichiometric, which potentially adds an additional layer of variety and dynamic control of mRNA metabolism. The m6A-modified mRNA can be selectively recognized by the YTH family “reader” proteins. The preferential binding of m6A-containing mRNA by YTHDF2 is known to reduce the stability of the target transcripts; however, the exact effects of m6A on translation has yet to be elucidated. Here we show that another m6A reader protein, YTHDF1, promotes ribosome loading of its target transcripts. YTHDF1 forms a complex with translation initiation factors to elevate the translation efficiency of its bound mRNA. In a unified mechanism of translation control through m6A, the YTHDF2-mediated decay controls the lifetime of target transcripts; whereas, the YTHDF1-based translation promotion increases the translation efficiency to ensure effective protein production from relatively short-lived transcripts that are marked by m6A. PAR-CLIP and RIP was used to identify YTHDF1 binding sites followed by ribosome profling and RNA seq to assess the consequences of YTHDF1 siRNA knock-down

2015-06-09 | E-GEOD-63591 | biostudies-arrayexpress

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