Effect of ILF3 depletion in HeLa cells on RNA steady state levels
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA540710 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9000470_1.fastq.gz | Fastqsanger.gz | |||
| SRR9000470_2.fastq.gz | Fastqsanger.gz | |||
| SRR9000471_1.fastq.gz | Fastqsanger.gz | |||
| SRR9000471_2.fastq.gz | Fastqsanger.gz | |||
| SRR9000472_1.fastq.gz | Fastqsanger.gz |
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Project description:Upon detection of viral infections, cells activate the expression of type I interferons (IFNs) and pro-inflammatory cytokines to control viral dissemination. As part of their antiviral response, cells also trigger the translational shutoff response which prevents translation of viral mRNAs and cellular mRNAs in a non-selective manner. Intriguingly, mRNAs encoding for antiviral factors bypass this translational shutoff, suggesting the presence of additional regulatory mechanisms enabling expression of the self-defence genes. Here, we identified the dsRNA binding protein ILF3 as an essential host factor required for efficient translation of the central antiviral cytokine, IFNB1, and a subset of interferon-stimulated genes. By combining polysome profiling and next-generation sequencing, ILF3 was also found to be necessary to establish the dsRNA-induced transcriptional and translational programs. We propose a central role for the host factor ILF3 in enhancing expression of the antiviral defence mRNAs in cellular conditions where cap-dependent translation is compromised. In this dataset we use polysome profiling in combination with RNA-seq to investigate the effect of ILF3 on the translation of mRNAs in HeLa cells in homeostasis and the antiviral response.
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