Ontology highlight
ABSTRACT:
PROVIDER: PRJNA630146 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11713582.fastq.gz | Fastqsanger.gz | |||
| SRR11713582_1.fastq.gz | Fastqsanger.gz | |||
| SRR11713582_2.fastq.gz | Fastqsanger.gz | |||
| SRR11713583_1.fastq.gz | Fastqsanger.gz | |||
| SRR11713583_2.fastq.gz | Fastqsanger.gz |
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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.
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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.
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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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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. HeLa cells transiently transfected with the pCAGGS vector for the control sample was compared with HeLa cells transiently transfected with the pCAGGS-Tax-FLAG vector. These cells were incubated for 30h after transfection and total RNA was isolated.
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