Illumina sequencing of PCR products derived from TBLV-induced tumors in the presence and absence of Rem
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ABSTRACT:
ORGANISM(S): Viruses
PROVIDER: GSE134189 | GEO | 2019/07/13
REPOSITORIES: GEO
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Project description:Illumina sequencing of PCR products derived from TBLV-induced tumors in the presence and absence of Rem
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Project description:Retroviruses cause lifelong infections resulting from their ability to thwart innate immunity. The Apobec family of cytidine deaminases are part of the innate immune response that recognizes and mutates foreign nucleic acids, including those from multiple viruses. Multiple retroviral antagonists of Apobecs have been identified, including mouse mammary tumor virus (MMTV)-encoded Rem protein. Previous experiments have shown that Rem-null MMTV or closely related TBLV proviruses from BALB/c tumors accumulate G-to-A and C-to-T mutations typical of Apobecs compared to wild-type proviruses expressing Rem. The difference in mutations between Rem-expressing and non-expressing MMTV strains largely disappeared in mice lacking the Apobec family member, activation-induced cytidine deaminase (AID). These results suggested that Rem is an AID antagonist. In this study, we attempted to study AID-mediated mutations of TBLV proviruses lacking Rem expression obtained from tumors in C57BL/6 (B6) wild-type and AID-knockout backgrounds. Surprisingly, no differences in G-to-A mutations were observed in TBLV proviruses regardless of Rem expression, yet such mutations were significantly reduced in proviruses obtained from mA3/AID-double knockout mice relative to those from wild-type B6 or AID-knockout mice. Many cellular mRNAs involving the innate immune response, but not Apobecs, were elevated in the absence relative to the presence of Rem expression on the B6 AID-knockout background. These results revealed that Apobec-mediated mutagenesis is dependent on mouse strain and suggested a second means of Rem-dependent immune evasion.
2024-04-15 | GSE263655 | GEO
Project description:Retroviruses cause lifelong infections resulting from their ability to thwart innate immunity. The Apobec family of cytidine deaminases are part of the innate immune response that recognizes and mutates foreign nucleic acids, including those from multiple viruses. Multiple retroviral antagonists of Apobecs have been identified, including mouse mammary tumor virus (MMTV)-encoded Rem protein. Previous experiments have shown that Rem-null MMTV or closely related TBLV proviruses from BALB/c tumors accumulate G-to-A and C-to-T mutations typical of Apobecs compared to wild-type proviruses expressing Rem. The difference in mutations between Rem-expressing and non-expressing MMTV strains largely disappeared in mice lacking the Apobec family member, activation-induced cytidine deaminase (AID). These results suggested that Rem is an AID antagonist. In this study, we attempted to study AID-mediated mutations of TBLV proviruses lacking Rem expression obtained from tumors in C57BL/6 (B6) wild-type and AID-knockout backgrounds. Surprisingly, no differences in G-to-A mutations were observed in TBLV proviruses regardless of Rem expression, yet such mutations were significantly reduced in proviruses obtained from mA3/AID-double knockout mice relative to those from wild-type B6 or AID-knockout mice. Many cellular mRNAs involving the innate immune response, but not Apobecs, were elevated in the absence relative to the presence of Rem expression on the B6 AID-knockout background. These results revealed that Apobec-mediated mutagenesis is dependent on mouse strain and suggested a second means of Rem-dependent immune evasion.
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Project description:<p>The ncRNA transcriptome of human hepatocellular carcinoma (HCC) is largely unexplored. We used CAGE to characterize transcription start sites across different etiologies of human HCCs with emphasis on ncRNAs. Here we report that retroviral LTR promoters, expressed in healthy tissues such as testis and placenta but not liver, are widely activated in HCC. Despite HCC heterogeneity, a subset of LTR-derived ncRNAs were more than 10-fold up-regulated in the vast majority of samples. HCCs with a high LTR activity mostly had a viral etiology, were less differentiated and showed higher risk of recurrence. CAGE enabled us to build a promoter map for HCC, which uncovers a new layer of complexity in HCC genomics.</p>
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Project description:96 BdbZIPs responding to 14 stresses were screened using qPCR. All samples were repeated with 3 times and GAPDH was regarded as house keeping gene. The stresses included heavy metal treatments, environmental factors and phytohormones
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Project description:An Excitatory Circuit in Perioculomotor Midbrain for Non-REM Sleep Control
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Project description:Three HCT116 cell lines (HCT WT, HCT p21-/-, HCT p53-/-) were analyzed by RT-qPCR array analysis for chromatin modification enzymes to identify potential target genes, that depend on the cell cycle regulator p21 and that are indpendent of p53. HCT116 cell lines (HCT WT, HCT p21-/-, HCT p53-/-) were cultured at 37°C in a humidified atmosphere with 5% CO2. Cells were harvested at a confluency of ~60-80% and RNA was isolatd using QIAzol an Rneasy Kits from Qiagen. cDNA was produced from equal amounts of RNA using the RT² First Strand Ki from Qiagen and RT-qPCR analysis was performed following the manufacturer's instructions using the Epigenetic Chromatin Modification Enzymes RT² Profiler PCR Array from Qiagen. The CFX96TM Real-Time System and the C1000TM Thermal Cycler from Bio-Rad were used to perform the RT-PCR runs. The three different cell lines were analyzed in three biological triplicates. The mean expression Ct values of the target genes were normalized against the mean Ct value for GAPDH to calculate the Fold Change values. The Raw Data was processed using the RT² Profiler PCR Array Data Analysis version 3.5 software from SABiosciences.
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