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

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

PROVIDER: PRJNA509686 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8314910_1.fastq.gz	Fastqsanger.gz
	SRR8314910_2.fastq.gz	Fastqsanger.gz
	SRR8314911_1.fastq.gz	Fastqsanger.gz
	SRR8314911_2.fastq.gz	Fastqsanger.gz
	SRR8314912_1.fastq.gz	Fastqsanger.gz

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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

KDR-dependent tyrosine phosphorylation in HTLV-1 transformed cells

Project description:Human T-cell leukemia virus type 1 (HTLV-1) is linked to the development of adult T-cell leukemia (ATL) and the neuroinflammatory disease, HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The HTLV-1 Tax oncoprotein regulates viral gene expression and the NF-kB pathway to promote the survival of HTLV-1 infected T cells. In thsi study, we utilize a kinome-wide shRNA screen to identify the tyrosine kinase KDR/VEGFR2 as an essential survival factor of HTLV-1-transformed T cells. Inhibition of KDR induces apoptosis of Tax expressing HTLV-1-transformed cell lines and CD4+ T cells from HAM/TSP patients. Phosphoproteomics analysis of HTLV-1 transformed cells treated with a KDR inhibitor revealed inhibition of the phosphorylation of multiple receptors/cell surface proteins, ubiquitin conjugating systems, proteases, phosphatases, apoptotic regulatory factors, adhesion/extracellular matrix proteins and viral proteins. This work suggests that HTLV-1 Tax has hijacked KDR kinase activity to promote Tax stability and the proliferation and survival of HTLV-1 infected cells.

2024-06-14 | PXD051981 | Pride

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

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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.

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Transcriptome-wide analysis of the role of HTLV-1 Tax PBM in T-Cells from infected humanized-mice (hu-Mice)

Project description:Human T-lymphotropic virus type 1 (HTLV-1) is associated with the development of Adult T-cell Leukemia, an aggressive CD4+ T-cells malignancy. Here, we have developed a new procedure to infect humanized mice with proviruses displaying specific mutations, such as one leading to the loss of the PDZ domain-binding motif (PBM) of Tax. In order to specifically analyze the in vivo role of the PBM of Tax, a comparative study of infected hu-mice was performed. We used next-generation sequencing to perform genome-wide transcriptomic analysis of T-cells infected with wild-type HTLV-1 virus or with virus bearing a mutated form of Tax lacking the PBM. Our results suggest that Tax PBM might be involved in the regulation of genes implicated in proliferation, apoptosis and cytoskeleton organization.

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2012-08-08 | E-GEOD-39986 | biostudies-arrayexpress

miRNA profiling of Jurkat with stably integrated HTLV1-LTR in the presence of HTLV-1 Tax

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Expression data from Human Tax transfected HeLa cell

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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

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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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