Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Viral hijacking of the TENT4-ZCCHC14 complex protects viral RNAs via mixed tailing [TAIL-seq]

ABSTRACT: TENT4 enzymes generate “mixed tails” on mRNAs by adding adenosines with intermittent non-adenosine residues, which protect mRNAs from deadenylation. Here we discover the extensive mixed tailing in the transcripts of two distinct DNA viruses, hepatitis B virus (HBV) and human cytomegalovirus (HCMV), and their striking similarity in the mechanism to exploit the TENT4-ZCCHC14 complex. TAIL-seq analyses of HBV and HCMV RNAs revealed that TENT4A and TENT4B are responsible for the mixed tailing and protection of viral poly(A) tails. By fCLIP-seq on HBV-producing cells, we found that the HBV posttranscriptional regulatory element (PRE) is the primary site of the TENT4 interactome. A hairpin with a CNGGN-type pentaloop in the PRE is critical for TENT4-dependent regulation. Unexpectedly, HCMV also utilizes a similar pentaloop hairpin, an interesting example of convergent evolution. We further found that the CNGGN pentaloop is recognized by the SAM domain-containing ZCCHC14 protein which in turn recruits TENT4 to stabilize viral transcripts. Altogether, our study reveals the action mechanism of PRE that has been widely used to enhance gene expression, and introduces the TENT4-ZCCHC14 complex as the key host factor and a potential target for antiviral therapeutics.

ORGANISM(S): Homo sapiens

PROVIDER: GSE146600 | GEO | 2020/03/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Viral hijacking of the TENT4-ZCCHC14 complex protects viral RNAs via mixed tailing

Project description:TENT4 enzymes generate “mixed tails” on mRNAs by adding adenosines with intermittent non-adenosine residues, which protect mRNAs from deadenylation. Here we discover the extensive mixed tailing in the transcripts of two distinct DNA viruses, hepatitis B virus (HBV) and human cytomegalovirus (HCMV), and their striking similarity in the mechanism to exploit the TENT4-ZCCHC14 complex. TAIL-seq analyses of HBV and HCMV RNAs revealed that TENT4A and TENT4B are responsible for the mixed tailing and protection of viral poly(A) tails. By fCLIP-seq on HBV-producing cells, we found that the HBV posttranscriptional regulatory element (PRE) is the primary site of the TENT4 interactome. A hairpin with a CNGGN-type pentaloop in the PRE is critical for TENT4-dependent regulation. Unexpectedly, HCMV also utilizes a similar pentaloop hairpin, an interesting example of convergent evolution. We further found that the CNGGN pentaloop is recognized by the SAM domain-containing ZCCHC14 protein which in turn recruits TENT4 to stabilize viral transcripts. Altogether, our study reveals the action mechanism of PRE that has been widely used to enhance gene expression, and introduces the TENT4-ZCCHC14 complex as the key host factor and a potential target for antiviral therapeutics.

2020-04-27 | PXD018061 | Pride

Viral hijacking of the TENT4-ZCCHC14 complex protects viral RNAs via mixed tailing [fCLIP-seq]

2020-03-09 | GSE146597 | GEO

Viral hijacking of the TENT4-ZCCHC14 complex protects viral RNAs via mixed tailing [fCLIP-seq]

Project description:Viral hijacking of the TENT4-ZCCHC14 complex protects viral RNAs via mixed tailing [fCLIP-seq]

| PRJNA611047 | ENA

Viral hijacking of the TENT4-ZCCHC14 complex protects viral RNAs via mixed tailing

Project description:Viral hijacking of the TENT4-ZCCHC14 complex protects viral RNAs via mixed tailing

| PRJNA611053 | ENA

Epitranscriptomic cytidine methylation of the Hepatitis B viral RNA encapsidation signal ensure the reverse transcription of viral RNA [RNA-Seq]

Project description:Epitranscriptomic RNA modifications have emerged as important regulators of the fate and function of both cellular and viral RNAs. One prominent modification, the cytidine methylation 5-methylcytidine (m5C), is found on the RNA of HIV-1, where m5C enhances the translation and splicing of HIV-1 RNA. However, whether m5C functionally enhances the RNA of other pathogenic viruses remain elusive. Here, we report that the RNA of hepatitis B virus (HBV) is enriched with a high level of m5C, mediated mainly through the cellular methyltransferase NSUN2. Intrigingly, the most prominent cluster of NSUN2-deposited m5C is found on the epsilon hairpin, an RNA element required for viral RNA encapsidation and reverse transcription. Loss of m5C from HBV RNA due to depletion of NSUN2 resulted in a modest decrease in viral capsid protein (HBc) translation, yet this is accompaneied by a near-complete loss of the reverse transcribed viral DNA. Similarly, mutations introduced to remove the methylated cytidines resulted in a translation decrease and block of reverse transcription. Furthermore, pharmacological disruption of m5C deposition with a nucleoside analogue led to a significant decrease in HBV replication. Thus, our data indicates m5C methylations is a critical enhancer of the epsilon element in HBV reverse transcription. Our study suggests the theraputic potential of targeting the m5C methyltransfer process on the HBV 5’epsilon as an alternative antiviral stratagy.

2024-05-20 | GSE250105 | GEO

Epitranscriptomic cytidine methylation of the Hepatitis B viral RNA encapsidation signal ensure the reverse transcription of viral RNA [PAR-CLIP]

2024-05-20 | GSE250108 | GEO

Epitranscriptomic cytidine methylation of the Hepatitis B viral RNA encapsidation signal ensure the reverse transcription of viral RNA [PA-m6A-seq]

2024-05-20 | GSE250107 | GEO

Epitranscriptomic cytidine methylation of the Hepatitis B viral RNA encapsidation signal ensure the reverse transcription of viral RNA [PA-m5C-seq]

2024-05-20 | GSE250106 | GEO

Epitranscriptomic cytidine methylation of the Hepatitis B viral RNA encapsidation signal ensure the reverse transcription of viral RNA [PA-m5C-seq 2]

2024-05-20 | GSE261877 | GEO

Viral hijacking of the TENT4-ZCCHC14 complex protects viral RNAs via mixed tailing [TAIL-seq]

Project description:Viral hijacking of the TENT4-ZCCHC14 complex protects viral RNAs via mixed tailing [TAIL-seq]

| PRJNA611056 | ENA