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

ABSTRACT: RNA interference (RNAi) is a natural cellular mechanism to silence gene expression and is predominantly mediated by microRNAs (miRNAs) that target messenger RNA. Viruses can manipulate the cellular processes necessary for their replication by targeting the host RNAi machinery. This study explores the effect of human T-cell leukemia virus type 1 (HTLV-1) transactivating protein Tax on the RNAi pathway in the context of a chromosomally integrated viral long terminal repeat (LTR) using a CD4(+) T-cell line, Jurkat.

ORGANISM(S): Homo sapiens

PROVIDER: GSE39986 | GEO | 2012/08/09

SECONDARY ACCESSION(S): PRJNA172209

REPOSITORIES: GEO

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

Project description:RNA interference (RNAi) is a natural cellular mechanism to silence gene expression and is predominantly mediated by microRNAs (miRNAs) that target messenger RNA. Viruses can manipulate the cellular processes necessary for their replication by targeting the host RNAi machinery. This study explores the effect of human T-cell leukemia virus type 1 (HTLV-1) transactivating protein Tax on the RNAi pathway in the context of a chromosomally integrated viral long terminal repeat (LTR) using a CD4(+) T-cell line, Jurkat. Jurkat cells with stably integrated HTLV1-LTR were transfected with either pCMV-Tax or pCMV. Total miRNA was isolated, labeled and hybridized to the miRNA microarray as described by the manufacturer (Invitrogen). The hybridized slides were then analyzed on a GenePix scanner.

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

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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.

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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.

2018-02-14 | GSE102220 | GEO

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.

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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

Functional difference in the HTLV-1 subgroup specific viral transcriptional regulators Tax

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2018-10-13 | GSE121201 | GEO

Transcription profiling of human CD4+ T-cell line Tesi in presence and absence 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. Experiment Overall Design: Tesi cells were kept in RPMI 1640 with 50% Panserin, 20% FCS, 0.35g/l glutamine, streptomycin as antibiotic and 40U/ml interleukin-2. To repress Tax expression, 1Âµg/ml tetracycline was added for ten days. Subsequently, total cellular RNA was extracted from samples and subjected to Affymetrix microarray analysis. For each state (with Tax and without Tax) a biological replicate was generated. Mean values of replicated samples were then compared.

2008-04-07 | E-GEOD-10508 | biostudies-arrayexpress

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