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Functional and molecular dissection of viral lncRNAs throughout HCMV life cycle

ABSTRACT: Functional and molecular dissection of viral lncRNAs throughout HCMV life cycle

PROVIDER: PRJNA900198 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22254169_1.fastq.gz	Fastqsanger.gz
	SRR22254169_2.fastq.gz	Fastqsanger.gz
	SRR22254170_1.fastq.gz	Fastqsanger.gz
	SRR22254170_2.fastq.gz	Fastqsanger.gz
	SRR22254171_1.fastq.gz	Fastqsanger.gz

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Functional and molecular dissection of viral lncRNAs throughout HCMV life cycle

Project description:Small, compact genomes confer a selective advantage to viruses, yet human cytomegalovirus (HCMV) expresses the long non-coding RNAs (lncRNAs) RNA1.2, RNA2.7, RNA4.9, and RNA5.0. These lncRNAs account for majority of the viral transcriptome, but their functions remain largely unknown. Here, we showed that HCMV lncRNAs, except for RNA5.0, are required throughout the entire viral life cycle. Deletion of each lncRNA resulted in a decrease in viral progeny during lytic replication and failing to efficiently establish latent reservoirs and reactivate. Nanopore direct RNA sequencing of native lncRNA molecules revealed that each lncRNA exhibited a dynamic modification landscape, depending on the state of infection. Global analysis of the lncRNA interactome identified 32, 11, and 89 host factors that specifically bind to RNA1.2, RNA2.7, and RNA4.9, respectively. Moreover, 52 proteins commonly bound to the three lncRNAs were identified, including 11 antiviral immunity-related proteins. Our molecular analyses found that three lncRNAs are modified with N⁶-methyladenosine (m6A) and interact with m6A readers in all infection states. In-depth functional analysis revealed that m6A–mediated lncRNA stabilization as the key mechanism by which lncRNAs are maintained at high levels. Our study lays the groundwork for understanding viral lncRNA–mediated regulation of host-virus interaction throughout the HCMV life cycle.

2022-11-14 | PXD034587 | Pride

Functional and molecular dissection of viral lncRNAs throughout HCMV life cycle [shortread]

Project description:Small, compact genomes confer a selective advantage to viruses, yet human cyto-megalovirus (HCMV) expresses the long non-coding RNAs (lncRNAs); RNA1.2, RNA2.7, RNA4.9, and RNA5.0. Little is known about the function of these lncRNAs in the virus life cycle. Here, we dissected the functional and molecular landscape of HCMV lncRNAs. We found that HCMV lncRNAs occupy ~30 % and 50~60 % of to-tal and poly(A)+ viral transcriptome, respectively, throughout virus life cycle. RNA1.2, RNA2.7, and RNA4.9, the three abundantly expressed lncRNAs, appear to be es-sential in all infection states. Among these three lncRNAs, depletion of RNA2.7 and RNA4.9 results in the greatest defect in maintaining latent reservoir and promoting lytic replication, respectively. Moreover, we delineated the global post-transcriptional nature of HCMV lncRNAs by nanopore direct RNA sequencing and interactome analysis. We revealed that the lncRNAs are modified with N⁶-methyladenosine (m6A) and interact with m6A readers in all infection states. In-depth analysis demonstrated that m6A machineries stabilize HCMV lncRNAs, which could account for the over-whelming abundance of viral lncRNAs. Our study lays the groundwork for under-standing the viral lncRNA–mediated regulation of host-virus interaction throughout the HCMV life cycle.

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Functional and molecular dissection of viral lncRNAs throughout HCMV life cycle [longread]

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Functional and molecular dissection of viral lncRNAs throughout HCMV life cycle [shortread]

Project description:Functional and molecular dissection of viral lncRNAs throughout HCMV life cycle [shortread]

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Functional and molecular dissection of viral lncRNAs throughout HCMV life cycle [longread]

Project description:Functional and molecular dissection of viral lncRNAs throughout HCMV life cycle [longread]

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Functional and molecular dissection of viral lncRNAs throughout HCMV life cycle

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Project description:Studying the effects of HIV infection on the host transcriptome has typically focused on protein-coding genes. However, recent advances in the field of RNA sequencing revealed that long non-coding RNAs (lncRNAs) add an extensive additional layer to the cell’s molecular network and are highly involved in the regulation of molecular processes, including gene expression. Here, we performed transcriptome profiling throughout a primary HIV infection in vitro to investigate lncRNA expression at the different HIV replication cycle processes (reverse transcription, integration and particle production). Subsequently, guilt-by-association, transcription factor and co-expression analysis were performed to infer biological roles for the lncRNAs identified in the HIV-host interplay. Many lncRNAs were shown to play a role in mechanisms relying on proteasomal and ubiquitinylation pathways, apoptosis, DNA damage responses and cell cycle regulation. Through transcription factor binding analysis, we found that lncRNAs display a distinct transcriptional regulation profile as compared to protein coding mRNAs, suggesting that mRNAs and lncRNAs are independently modulated from each other. In addition, we identified five differentially expressed lncRNA-mRNA pairs with mRNA involvement in HIV pathogenesis (HIV linked co-expression) with possible cis regulatory lncRNAs that control the nearby mRNA expression and function. Altogether, the present study demonstrates that lncRNAs add a new dimension to the HIV-host interplay and should be further investigated as they may represent targets for controlling HIV replication.

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