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The viral oncoproteins Tax and HBZ control the host mRNA splicing landscape

ABSTRACT: The viral oncoproteins Tax and HBZ control the host mRNA splicing landscape

PROVIDER: PRJNA609707 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11214755_1.fastq.gz	Fastqsanger.gz
	SRR11214755_2.fastq.gz	Fastqsanger.gz
	SRR11214756_1.fastq.gz	Fastqsanger.gz
	SRR11214756_2.fastq.gz	Fastqsanger.gz
	SRR11214757_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

The viral oncoproteins Tax and HBZ control the host mRNA splicing landscape

Project description:We demonstrate that the HTLV-1 oncoviral proteins Tax and HBZ differentially alter the transcriptome landscape in T-cells

2021-09-13 | GSE146210 | GEO

The HTLV-1 viral oncoproteins Tax and HBZ reprogram the cellular mRNA splicing landscape.

Project description:Viral infections are known to hijack the transcription and translation of the host cell. However, the extent to which viral proteins coordinate these perturbations remains unclear. Here we used a model system, the human T-cell leukemia virus type 1 (HTLV-1), and systematically analyzed the transcriptome and interactome of key effectors oncoviral proteins Tax and HBZ. We showed that Tax and HBZ target distinct but also common transcription factors. Unexpectedly, we also uncovered a large set of interactions with RNA-binding proteins, including the U2 auxiliary factor large subunit (U2AF2), a key cellular regulator of pre-mRNA splicing. We discovered that Tax and HBZ perturb the splicing landscape by altering cassette exons in opposing manners, with Tax inducing exon inclusion while HBZ induces exon exclusion. Among Tax- and HBZ-dependent splicing changes, we identify events that are also altered in Adult T cell leukemia/lymphoma (ATLL) samples from two independent patient cohorts, and in well-known cancer census genes. Our interactome mapping approach, applicable to other viral oncogenes, has identified spliceosome perturbation as a novel mechanism coordinated by Tax and HBZ to reprogram the transcriptome.

| S-EPMC8483338 | biostudies-literature

Intragenic recruitment of NF-kB drives splicing modifications upon activation by the oncogene Tax of HTLV-1

Project description:Chronic NF-kB activation in inflammation and cancer has long been linked to persistent activation of NF-kB–responsive gene promoters. However, NF-kB factors also massively bind to gene bodies. Here, we demonstrate that recruitment of the NF-kB factor RELA to intragenic regions regulates alternative splicing upon NF-kB activation by the viral oncogene Tax of HTLV-1. Integrative analyses of RNA splicing and chromatin occupancy, combined with chromatin tethering assays, demonstrate that DNA-bound RELA interacts with and recruits the splicing regulator DDX17, in an NF-kB activation–dependent manner. This leads to alternative splicing of target exons due to the RNA helicase activity of DDX17. Similar results were obtained upon Tax-independent NF-kB activation, indicating that Tax likely exacerbates a physiological process where RELA provides splice target specificity. Collectively, our results demonstrate a physical and direct involvement of NF-kB in alternative splicing regulation, which significantly revisits our knowledge of HTLV-1 pathogenesis and other NF-kB–related diseases.

2020-05-12 | GSE123752 | GEO

Profile of gene expression in Tax positive (TaxP) cells compared with Tax negative (TaxN) cells.

Project description:Investigating the effect of Tax protein on the expression of genes in Jurkat cells. Current study will help us to elucidate the differential gene expression profiles of Tax positive Jurkat cells. The Tax-positive (TaxP) and Tax negative (TaxN) subline of Jurkat were established. mRNA isolated from TaxN or TaxP cell lines were analyzed using gene array.

2012-07-26 | E-GEOD-39601 | biostudies-arrayexpress

Profile of gene expression in Tax positive (TaxP) cells compared with Tax negative (TaxN) cells.

2012-07-27 | GSE39601 | GEO

Transcriptome analysis of HTLV-1 Tax-transformed T cell line Tesi in absence and presence of Tax

Project description:The Tesi system allows analysis of HTLV-1 Tax's impact on the transcriptome of a human CD4+ T-cell which is not derived from leukemia but directly from normal human lymphocytes. By comparing cells with and without Tax, one can specifically filter for celluar genes that are either activated or repressed in the presence of Tax. Keywords: cell type comparison, Tax

2008-02-14 | GSE10508 | GEO

RNA sequencing for transcriptome comparison between HTLV-1 Tax(-) and Tax(+) cells in Adult T-cell leukemia cell lines (MT-1 and KK-1)

Project description:Initially, ATL cell lines (MT-1 or KK-1) were stably transfected with reporter plasmid for HTLV-1 Tax expression, and single clones were isolated . This reporter in composed of Tax responsive element upstream of d2EGFP fluorescent protein. d2EGFP is expressed upon Tax expression in any individual cell. To compare transcriptomes of Tax(-) and Tax(+) cells, FACS sorting was done for d2EGFP(-) and d2EGFP(+) populations and RNA sequencing was performed.

2018-02-02 | GSE108601 | GEO

The endogenous HBZ interactome in ATL leukemic cells reveals an unprecedented complexity of host interacting partners involved in RNA splicing

Project description:Five percent of HTLV-1 infected subjects develops an untreatable form of cancer designated Adult T cell leukemia (ATL). The HTLV-1-encoded HBZ protein is believed to act as a viral oncogene by disarranging crucial pathways in the infected cells. Key to thisfunction is a progressive cytoplasmic-to-nuclear dislocation of HBZ and its interaction with nuclear factors whose complexity wasnot assessed until now. In this investigation we unveiled for the first time such complexity by studying the endogenous HBZinteractome in a leukemic cell line derived from an ATL patient. A high number of nuclear interactors, represented by at least 249members, were found. Among the various family of interactors, we found predominant the family involved in RNA splicing and RNAstability. A disarrangement of the splicing mechanism was demonstrated both in ATL cells and in non HTLV-1-derived leukemic cellsexpressing HBZ after genetic transfer, strongly suggesting that a major mechanism leading to HTLV-1-mediated transformationand persistence of the oncogenic state is related to this event. Our unprecedented results shed new light on the mechanisms bywhich a human retrovirus can alter the infected cell metabolism and strongly predispose and/or maintain neoplastictransformation

2022-07-27 | GSE206085 | GEO

Expression data from Human Tax transfected HeLa cell

2013-03-21 | GSE34750 | GEO

Expression data from Human Tax transfected HeLa cell

Project description:Human T cell leukemia virus type 1 (HTLV-1) Tax is potent activator of viral and cellular gene expression that interacts with a number of cellular proteins. In this study, a large-scale host cell signaling events related to cellular proliferation were used to identify genes involved in Tax-mediated cell signaling events related to cellular proliferation and apoptosis. HeLa cell transiently transfected with with pCAGGS vector for control sample was compared with HeLa cell transiently transfected with with pCAGGS-Tax-FLAG vector. These cells were incubated for 30h after transfection and were used for total RNA isolation.

2013-03-21 | E-GEOD-34750 | biostudies-arrayexpress

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