Bovine Leukemia Virus (BLV) antisense transcripts
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB13872 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1398270_1.fastq.gz | Fastqsanger.gz | |||
| ERR1398270_2.fastq.gz | Fastqsanger.gz | |||
| ERR1399610.fastq.gz | Fastqsanger.gz | |||
| ERR1399610_1.fastq.gz | Fastqsanger.gz | |||
| ERR1399610_2.fastq.gz | Fastqsanger.gz |
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Project description:In sheep infected with bovine leukemia virus (BLV), transcription of structural, enzymatic, and accessory genes is silenced. However, the BLV provirus transcribes a series of non-coding RNAs that remain undetected by the host immune response. Specifically, three RNAs (AS1-L, AS1-S, and AS2) are consistently expressed from the antisense strand, originating from transcriptional initiation at the 3'-LTR. To investigate the role of these non-coding RNAs in viral replication and pathogenesis, a reverse genetics approach was devised, capitalizing on a mechanistic disparity in transcription initiation between the 5' and 3' promoters. A two-nucleotide mutation (GG>TA) in the TFIIB-recognition element (BRE) impaired antisense transcription originating from the 3'-LTR. In the context of the provirus, this A1 mutation significantly diminished the expression of antisense RNAs, while not notably affecting sense transcription. When inoculated to sheep, the A1 provirus was infectious but exhibited reduced replication levels, shedding light on the role of antisense transcription in vivo. In comparison to lymphoid organs in sheep infected with a wild-type (WT) provirus, the A1 mutant demonstrated alterations in both the spatial distribution and rates of cell proliferation in the lymph nodes and the spleen. Analysis through RNA sequencing and RT-qPCR unveiled an upregulation of the Hmcn1 gene in B-lymphocytes from A1-infected sheep. Further examination via confocal microscopy and immunohistochemistry revealed an increase in the amount of hemicentin-1 protein encoded by Hmcn1 in peripheral blood mononuclear cells (PBMCs) and lymphoid organs of sheep infected with the A1 mutant. RNA interference targeting Hmcn1 expression impacted the migration of ovine kidney (OVK) cells in vitro. In contrast to the WT provirus, the A1 mutant lacked oncogenic activity when inoculated into sheep. Collectively, this study underscores the essential role of antisense transcription in BLV replication and pathogenicity. These findings may offer valuable insights into understanding the relevance of antisense transcription in the context of human T-cell leukemia virus (HTLV-1).
2024-02-17 | GSE255715 | GEO
Project description:Background: Bovine leukemia virus (BLV) microRNAs (miRNAs) contribute to viral latency and immune evasion. Naturally occurring single-nucleotide polymorphisms (SNPs) within the BLV miRNA cluster have been associated with persistent lymphocytosis in cattle, yet their functional impact remains unclear. Aims: This study aims to (1) evaluate how SNPs in BLV miRNAs affect miRNA biogenesis and mature miRNA levels; (2) determine whether specific SNPs alter miRNA–mRNA interactions and identify affected targets; and (3) characterize transcriptomic changes induced by reference versus SNP-bearing miRNAs. Methods: BLV miRNA loci were PCR-amplified and sequenced from 53 blood samples of infected cattle. Both reference and SNP-containing precursors were cloned into expression vectors and co-transfected with an miRNA-deficient BLV clone into HEK293T cells. Mature miRNA levels were quantified via stem-loop RT-qPCR. Computational target prediction (miRanda) validated changes in mRNA targeting. Gene-expression effects were assessed using Agilent microarrays, with selected findings confirmed by RT-qPCR and subjected to pathway enrichment analysis (IPA). Significance: This work will elucidate how BLV miRNA polymorphisms modify miRNA maturation and target recognition, reshape host gene networks, and contribute to viral persistence and immune modulation.
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Project description:This SuperSeries is composed of the following subset Series: GSE14372: Novel endogenous antisense transcripts (data for the mouse normal tissues) GSE14557: Novel endogenous antisense transcripts (data for the mouse mammary tumors) Refer to individual Series Unpublished data has been masked in the supplementary feature extraction files.
2009-08-24 | E-GEOD-14568 | biostudies-arrayexpress
Project description:The positioning of the nucleosome by ATP-dependent nucleosome remodelers provides the fundamental chromatin environment for the regulation of diverse cellular processes acting on the underlying DNA. Here, we report that the fission yeast CHD remodeler, Hrp3, is a global regulator that drives higher-order chromatin structure and genomic stability. The loss of Hrp3 resulted in the production of antisense transcripts and perturbation of the nucleosome in an ATPase mutant of Hrp3 was also associated with destabilization of the DNA-histone interaction. Furthermore, the effect of Hrp3 in the pericentric region was found to be accomplished via a physical interaction with Swi6, and appeared to cooperate with other heterochromatin factors for gene silencing. Taken together, our data indicate that a well-positioned nucleosome is important for the spatial-temporal control of transcription-associated processes, and show that this is accomplished by the chromatin remodeler, Hrp3, in fission yeast. Two-condition experiment, Mutant vs Wild-type (control)
2012-05-07 | E-GEOD-37697 | biostudies-arrayexpress
Project description:Intronic natural antisense transcripts in glioma patient biopsies
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Project description:Bovine leukaemia virus (BLV) is a retrovirus that infects cattle, causing Bovine Enzootic Leukosis, a chronic disease characterized by the proliferation of infected B cells. BLV proviral load (PVL) is a key determinant of disease progression and transmission risk. Cattle can exhibit distinct phenotypes of low PVL (LPVL) or high PVL (HPVL), which remain stable throughout their lifetime. Differential expression analysis performed in edgeR identified 1,908 differentially expressed genes (DEGs) between HPVL and LPVL animals, including 774 downregulated (DReg) and 1134 upregulated (UReg) genes.
2025-03-28 | GSE282244 | GEO
Project description:The positioning of the nucleosome by ATP-dependent nucleosome remodelers provides the fundamental chromatin environment for the regulation of diverse cellular processes acting on the underlying DNA. Here, we report that the fission yeast CHD remodeler, Hrp3, is a global regulator that drives higher-order chromatin structure and genomic stability. The loss of Hrp3 resulted in the production of antisense transcripts and perturbation of the nucleosome in an ATPase mutant of Hrp3 was also associated with destabilization of the DNA-histone interaction. Furthermore, the effect of Hrp3 in the pericentric region was found to be accomplished via a physical interaction with Swi6, and appeared to cooperate with other heterochromatin factors for gene silencing. Taken together, our data indicate that a well-positioned nucleosome is important for the spatial-temporal control of transcription-associated processes, and show that this is accomplished by the chromatin remodeler, Hrp3, in fission yeast.
2012-05-08 | GSE37697 | GEO
Project description:Bovine Leukemia Virus (BLV)-induced tumoral development is a multifactorial phenomenon which remains incompletely understood. Here, we highlight the critical role of the cellular CCCTC-binding factor (CTCF) both in the regulation of BLV transcriptional activities and in the deregulation of the three-dimensional (3D) chromatin architecture surrounding the BLV integration site. We demonstrated the in vivo recruitment of CTCF to three conserved CTCF binding motifs along the BLV provirus. Next, we showed the localization of CTCF to transitions in the histone modifications profile along BLV genome as well as its implication in the repression the 5’Long Terminal Repeat (LTR) promoter activity, thereby contributing to viral latency, while favoring the 3’LTR promoter activity. Finally, we demonstrated that BLV integration deregulated host cellular 3D chromatin organization through the formation of viral/host chromatin loops. Altogether, our results highlight CTCF as a new critical effector of BLV transcriptional regulation and BLV-induced physiopathology.
2022-02-18 | GSE178482 | GEO
Project description:Bovine Leukemia Virus (BLV)-induced tumoral development is a multifactorial phenomenon which remains incompletely understood. Here, we highlight the critical role of the cellular CCCTC-binding factor (CTCF) both in the regulation of BLV transcriptional activities and in the deregulation of the three-dimensional (3D) chromatin architecture surrounding the BLV integration site. We demonstrated the in vivo recruitment of CTCF to three conserved CTCF binding motifs along the BLV provirus. Next, we showed the localization of CTCF to transitions in the histone modifications profile along BLV genome as well as its implication in the repression the 5’Long Terminal Repeat (LTR) promoter activity, thereby contributing to viral latency, while favoring the 3’LTR promoter activity. Finally, we demonstrated that BLV integration deregulated host cellular 3D chromatin organization through the formation of viral/host chromatin loops. Altogether, our results highlight CTCF as a new critical effector of BLV transcriptional regulation and BLV-induced physiopathology.
2022-02-18 | GSE178483 | GEO
Project description:Bovine leukemia virus (BLV) Tax is a transcriptional activator of viral replication and a key contributor to oncogenic potential. We previously identified interesting mutant forms of Tax with elevated (TaxD247G) or reduced (TaxS240P) transactivation effects on BLV replication and propagation. In this study, to identify genes that play a role in the cascade of signal events regulated by wild-type and mutant Tax proteins, we used a large-scale host cell gene-profiling approach.
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