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Genome-wide binding map of the HIV Tat protein to the human genome (ChIP-Seq)

ABSTRACT: The HIV-1 Trans-Activator of Transcription (Tat) protein binds to multiple host cellular factors and greatly enhances the level of transcription of the HIV genome. Here, we report the genome-wide binding map of Tat to the human genome in Jurkat T cells (Jurkat-Tat cells) using chromatin immunoprecipitation combined with next-generation sequencing. cDNA microarray was used to monitor gene expression changes between Jurkat and Jurkat-Tat cells. Additionally, we compared distribution of H3K9ac near gene promoters between Jurkat and Jurkat-Tat cells using ChIP-chip method and hybridized onto Agilent promoter array. Our data reveal that Tatâs interaction with the host genome is more extensive than previously thought, with potentially important implications for the viral life cycle.

ORGANISM(S): Homo sapiens

PROVIDER: GSE30738 | GEO | 2011/11/06

SECONDARY ACCESSION(S): PRJNA154551

REPOSITORIES: GEO

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Genome-wide binding map of the HIV Tat protein to the human genome (gene expression)

Project description:The HIV-1 Trans-Activator of Transcription (Tat) protein binds to multiple host cellular factors and greatly enhances the level of transcription of the HIV genome. Here, we report the genome-wide binding map of Tat to the human genome in Jurkat T cells (Jurkat-Tat cells) using chromatin immunoprecipitation combined with next-generation sequencing. cDNA microarray was used to monitor gene expression changes between Jurkat and Jurkat-Tat cells. Additionally, we compared distribution of H3K9ac near gene promoters between Jurkat and Jurkat-Tat cells using ChIP-chip method and hybridized onto Agilent promoter array. Our data reveal that Tat’s interaction with the host genome is more extensive than previously thought, with potentially important implications for the viral life cycle. Agilent gene expression microarray was used to compare gene expression changes between Jurkat T cells and Jurkat T cells expressing HIV-Tat protein (Jurkat-Tat T cells) Expression profiles on Jurkat-Tat cells versus Jurkat cells. ChIP on chip for H3K9ac in Jurkat-Tat versus Jurkat cells. ChIP-seq for HIV-1 Tat protein in Jurkat-Tat cells.

2011-11-06 | E-GEOD-30734 | biostudies-arrayexpress

Genome-wide binding map of the HIV Tat protein to the human genome (ChIP-chip)

Project description:The HIV-1 Trans-Activator of Transcription (Tat) protein binds to multiple host cellular factors and greatly enhances the level of transcription of the HIV genome. Here, we report the genome-wide binding map of Tat to the human genome in Jurkat T cells (Jurkat-Tat cells) using chromatin immunoprecipitation combined with next-generation sequencing. cDNA microarray was used to monitor gene expression changes between Jurkat and Jurkat-Tat cells. Additionally, we compared distribution of H3K9ac near gene promoters between Jurkat and Jurkat-Tat cells using ChIP-chip method and hybridized onto Agilent promoter array. Our data reveal that Tat’s interaction with the host genome is more extensive than previously thought, with potentially important implications for the viral life cycle. Expression profiles on Jurkat-Tat cells versus Jurkat cells. ChIP on chip for H3K9ac in Jurkat-Tat versus Jurkat cells. ChIP-seq for HIV-1 Tat protein in Jurkat-Tat cells.

2011-11-06 | E-GEOD-30736 | biostudies-arrayexpress

Genome-wide binding map of the HIV Tat protein to the human genome (ChIP-Seq)

Project description:The HIV-1 Trans-Activator of Transcription (Tat) protein binds to multiple host cellular factors and greatly enhances the level of transcription of the HIV genome. Here, we report the genome-wide binding map of Tat to the human genome in Jurkat T cells (Jurkat-Tat cells) using chromatin immunoprecipitation combined with next-generation sequencing. cDNA microarray was used to monitor gene expression changes between Jurkat and Jurkat-Tat cells. Additionally, we compared distribution of H3K9ac near gene promoters between Jurkat and Jurkat-Tat cells using ChIP-chip method and hybridized onto Agilent promoter array. Our data reveal that TatM-CM-"M-BM-^@M-BM-^Ys interaction with the host genome is more extensive than previously thought, with potentially important implications for the viral life cycle. Expression profiles on Jurkat-Tat cells versus Jurkat cells. ChIP on chip for H3K9ac in Jurkat-Tat versus Jurkat cells. ChIP-seq for HIV-1 Tat protein in Jurkat-Tat cells.

2011-11-06 | E-GEOD-30738 | biostudies-arrayexpress

Genome-wide binding map of the HIV Tat protein to the human genome (gene expression)

2011-11-06 | GSE30734 | GEO

Genome-wide binding map of the HIV Tat protein to the human genome (ChIP-chip)

2011-11-06 | GSE30736 | GEO

Genome-wide binding map of the HIV Tat protein to the human genome

Project description:This SuperSeries is composed of the following subset Series: GSE30734: Genome-wide binding map of the HIV Tat protein to the human genome (gene expression) GSE30736: Genome-wide binding map of the HIV Tat protein to the human genome (ChIP-chip) GSE30738: Genome-wide binding map of the HIV Tat protein to the human genome (ChIP-Seq) Refer to individual Series

2011-11-06 | E-GEOD-30739 | biostudies-arrayexpress

Profiling of genes deregulated in CD4+ T cells expressing constitutively full-length or first-exon Tat protein of HIV-1

Project description:Background: The role of HIV-1 Tat protein in gene expression deregulation and functional biology of CD4+ T lymphocytes was analyzed, as well as the function of Tat second exon for the complete activity of this protein. Gene expression deregulation profiles of triplicate samples from Jurkat cells expressing intracellular full-length Tat (1-101aa) in comparison with a truncated form lacking the second exon (1-72aa) was evaluated by bioinformatics using whole human genome microarrays. Results: More than 1000 genes were deregulated in Jurkat Tat101 cells, whereas less than 300 genes were deregulated in Jurkat Tat72 cells (q-value<5%; fold change >2 or <-2). Ontological analysis indicated that several functions were impaired mainly in Jurkat Tat101 as cellular movement, growth and proliferation, cell-to-cell signaling, molecular transport, cell death, cell morphology, and T-cell activation. In accordance, biological and functional analyses proved that Tat101 intracellular expression induced changes in cell size and complexity, cytoskeletal rearrangements and chemotaxis impairment, higher resistance to apoptosis, decrease in the surface expression of adhesion molecules and receptors, and higher basal transcriptional activation. These alterations were attenuated or absent in Jurkat Tat72 cells. Furthermore, computational modeling showed that the absence of second exon severely reduced the C-terminus of Tat72 with notable decrease of positive charging. Conclusion: Full-length Tat intracellular expression induced dramatic structural changes and impaired essential functions in CD4+ T cells, whereas Tat72 was less aggressive. Consequently, although Tat first exon is transcriptionally autonomous, second exon should be indispensable for triggering HIV-1 pathogenic events induced by Tat protein. Keywords: Microarray Genome-wide expression analysis. Comparison of genetically modified cells

2010-01-29 | GSE20088 | GEO

Changes in the MicroRNA Expression Pattern Contribute to HIV-1 Tat-mediated Protection against Apoptosis and Impaired Cell Proliferation in CD4+ T Cells

Project description:HIV-1 infection changes the miRNA expression pattern in CD4+ T lymphocytes and its main regulator, Tat, has been appointed as an RNA silencing suppressor (RSS). Our group previously described that full-length Tat protects CD4+ T cells against FasL-mediated apoptosis and delays T-cell proliferation. Now we analyzed by microarrays and qRT-PCR the changes in the miRNA expression pattern of Jurkat cells induced by the intracellular expression of the two-exon Tat101 protein or the first-exon Tat72 in order to elucidate their role in the anti-apoptotic and anergic state exerted by Tat. It was determined that the expression of specific miRNAs such as hsa-miR-21, hsa-miR-222, hsa-miR-29a, and hsa-miR-1290 was up-regulated in Jurkat-Tat101. These miRNAs were related to the high activity of several transcription factors related to Tat such as NF-kB, SP1 and STAT3, and they repressed the expression of target mRNAs encoding proteins related to apoptosis and cell proliferation such as PTEN, PDCD4 and CDKN1B. In fact, mostly Jurkat-Tat101 showed an arrest at G2 phase and an impaired cytokinesis, resulting in giant, multilobulated nuclear cells. All these mechanisms would contribute to the role of Tat in HIV-1 immunosuppression and persistent infection, and the presence of Tat second exon would be essential.

2017-11-09 | GSE48800 | GEO

ChIP-chip from KG-1 cells with HIV Tat

Project description:HIV-1 Tat can modulate the expression of both HIV and cellular genes. In antigen-presenting cells Tat induces the expression of a subset of interferon-stimulated genes (ISGs) in the absence of interferons (IFNs). We investigated the genome-wide Tat association with cellular promoters in immature dendritic cells (iDC) and in monocyte derived macrophages (MDM). Chromatin immunoprecipitation (ChIP) of Tat together with chromatin profiling by ChIP-on-chip analysis demonstrated that Tat associates with the MAP2K6 and MAP2K3 promoters and mediates its increase, which also affects the induction of some ISGs.

2013-05-31 | GSE42191 | GEO

Tat RNA silencing suppressor activity contributes to perturbation of lymphocyte miRNAs by HIV-1

Project description:Herein expression trends of host miRNA were measured in CEMx174 lymphocytes infected with HIV-1NL4-3 or derivative strains deficient in Tat RSS activity (RSS) or vif-/vpr (VV), or unexposed to virus. As expected from previous studies, miRNA trends were different in naive and HIV-1 infected cells. Moreover, miRNA expression trends were similar for HIV-1 and vif-/vpr-deficient HIV-1, but diverged for RSS. Rather than generalized changes in miRNA levels, HIV-1 bearing the Tat K51A RSS mutation changed the steady state of a subset of miRNAs. The results are attributable to reduction in miRNA stability or change in miRNAs activity that altered steady state expression. Comparison of the miRNA expression trends in patient PBMC and the CEMx174 lymphocytes determined >50% overlap with a subset of miRNAs identified in patients, supporting the utility of HIV-1 cell culture model to refine experimental design with patient samples, which represent miRNA profiles of co-isolated infected and uninfected cells. Our results indicate that ablation of Tat RNA silencing suppressor activity in HIV-1 changes the steady state of a subset of host mature miRNA. The observation reinforces the concept of active HIV-1 interplay with host small RNAs that modulate replication and spread. The study validated the utility of derivative HIV-1 strains to explore the interface of viral genes with host small RNA activity. In this study the microRNA profiles of CEMx174 cells infected with HIV-1 NL4-3 or derivative viruses deficient in Vif/Vpr or Tat RNA silencing suppressor activity were compared to mock infected cells. The samples were analyzed in duplicate.

2011-03-01 | E-GEOD-21892 | biostudies-arrayexpress

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