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SARS-CoV-2 ORF6 disrupts innate immune signalling by inhibiting cellular mRNA export

ABSTRACT: SARS-CoV-2 ORF6 disrupts innate immune signalling by inhibiting cellular mRNA export

PROVIDER: PRJEB49943 | ENA |

REPOSITORIES: ENA

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SARS-CoV-2 ORF6 disrupts innate immune signalling by inhibiting cellular mRNA export.

Project description:SARS-CoV-2 is a betacoronavirus and the etiological agent of COVID-19, a devastating infectious disease. Due to its far-reaching effect on human health, there is an urgent and growing need to understand the viral molecular biology of SARS-CoV-2 and its interaction with the host cell. SARS-CoV-2 encodes 9 predicted accessory proteins, which are presumed to be dispensable for in vitro replication, most likely having a role in modulating the host cell environment to aid viral replication. Here we show that the ORF6 accessory protein interacts with cellular Rae1 to inhibit cellular protein production by blocking mRNA export. We utilised cell fractionation coupled with mRNAseq to explore which cellular mRNA species are affected by ORF6 expression and show that ORF6 can inhibit the export of many mRNA including those encoding antiviral factors such as IRF1 and RIG-I. We also show that export of these mRNA is blocked in the context of SARS-CoV-2 infection. Together, our studies identify a novel mechanism by which SARS-CoV-2 can manipulate the host cell environment to supress antiviral responses, providing further understanding to the replication strategies of a virus that has caused an unprecedented global health crisis.

| S-EPMC9451085 | biostudies-literature

Latent HIV infection disrupts cell-intrinsic innate immunity

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Signalling inhibition by ponatinib disrupts alternative lengthening of telomeres (ALT)

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Obesity disrupts innate-adaptive immune network patterning in adipose tissue

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Latent HIV infection disrupts cell-intrinsic innate immunity [scRNA-seq]

Project description:Latent HIV infection disrupts cell-intrinsic innate immunity [scRNA-seq]

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Vitamin D modulation of innate immune signalling in Dendritic Cells

Project description:Vitamin D is widely reported to inhibit innate immune signalling and dendritic cell (DC) maturation, leading to attenuation of DC mediated T cell activation as a potential immunoregulatory mechanism to guard against autoimmunity and immmunopathology. It is not known whether vitamin D has global or gene specific effects on transcriptional responses downstream of innate immune stimulation. In order to address this question, we used genome-wide transcriptional profiling of monocyte derived DC differentiated in the presence and absence of vitamin D, and then stimulated with and without lipopolysaccharide for four hours.

2016-10-03 | E-MTAB-4883 | biostudies-arrayexpress

Canonical Wnt signalling regulates nuclear export of Setdb1 during skeletal muscle terminal differentiation [ChIP-seq]

Project description:The histone 3 lysine 9 (H3K9)-specific methyltransferase (KMT) Setdb1 is essential for both stem cell pluripotency and terminal differentiation of different cell types. To shed light on Setdb1 role(s) in these mutually exclusive processes, we used mouse skeletal myoblasts as a model of terminal differentiation. Ex vivo studies on isolated single myofibres showed that Setdb1 is required for muscle adult stem cells expansion following activation and in vitro studies on skeletal myoblasts confirmed that Setdb1 suppresses terminal myoblast differentiation. We used genome-wide analyses to identify Setdb1 direct target genes in myoblasts and observed a release of Setdb1 from the promoter of selected target genes upon myoblast terminal differentiation, concomitant to a nuclear export of Setdb1 to the cytoplasm. We demonstrated that both genomic release and cytoplasmic Setdb1 relocalisation during differentiation were dependent on canonical Wnt signalling. Taken together, our findings uncover a functional link between Setdb1 and canonical Wnt signalling in skeletal muscle cells, which affects the expression of a subset of Setdb1 target genes. We revealed Wnt-dependent subcellular relocalisation of Setdb1 as a novel mechanism regulating Setdb1 functions. ChIP-seq of Setdb1 and H3K9me3 in Myoblast cells (C2C12)

2016-02-01 | E-GEOD-65493 | biostudies-arrayexpress

Mefloquine disrupts cancer stem cells by inhibiting lysosomal RAB5/7 mediated mitophagy

Project description:Mefloquine disrupts cancer stem cells by inhibiting lysosomal RAB5/7 mediated mitophagy

| PRJNA476805 | ENA

Canonical Wnt signalling regulates nuclear export of Setdb1 during skeletal muscle terminal differentiation

Project description:Canonical Wnt signalling regulates nuclear export of Setdb1 during skeletal muscle terminal differentiation

| PRJNA287564 | ENA

Wnt signalling in colon cancer

Project description:Hypothesis and proof of concept: Our hypothesis is that increase in cellular iron import proteins (TfR1, DMT1) occur early in the adenoma-carcinoma sequence through mutations in APC and lead to cellular iron loading. As demonstrated in our previous work the effects of this iron loading is to mediate increased Wnt signalling resulting in c-myc induction. This in turn serves to increase the expression of iron import proteins (TfR1, DMT1) and decrease the expression of iron export (ferroportin [FPN]) and storage (ferritin) proteins. Such a hypothesis explains how Wnt signalling controls iron metabolism and ensures that there is adequate cellular iron for ATP generation and cellular proliferation. Experimental design: To test such a hypothesis we aim to prospectively collect the following colorectal tissue from patients attending for colonoscopy: 1. Normal colonic mucosa in patients with no colorectal pathology (n = 30) 2. Polyps and matched normal colon (n = 30) 3. Colorectal cancers and matched normal colon (n = 30) We also intend to collect serum and urine from the following patient groups: 4. Normal colonoscopy (n = 30) 5. Colorectal adenomas (n = 30) 6. Colorectal cancers (n = 30) Primary outcome(s): Measured at baseline, using the expression of proteins in the tissue and serum to detect the cellular and systemic iron transport proteins. The techniques used will include mass spectrometry, western blotting, real time PCR and immunohistochemistry.

| 2416626 | ecrin-mdr-crc

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