Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1168660 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30881861_1.fastq.gz | Fastqsanger.gz | |||
| SRR30881861_2.fastq.gz | Fastqsanger.gz |
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Project description:Polyglutamine expansion is associated with pathogenic protein aggregation in neurodegenerative disorders. However, long polyglutamine tracts are also found in many transcription factors (TFs), such as FOXP2, a TF implicated in human speech. Here, we explore how FOXP2 and other glutamine-rich TFs avoid unscheduled assembly. Throughout interphase, DNA binding, irrespective of sequence specificity, has a solubilizing effect. During mitosis, multiple phosphorylation events promote FOXP2’s eviction from chromatin and supplant the solubilizing function of DNA. Further, human-specific amino-acid substitutions linked to the evolution of speech map to a mitotic phospho-patch, the ‘EVO patch’, and reduce the propensity of the human FOXP2 to assemble. Fusing the pathogenic form of Huntingtin to either a DNA binding domain, a phospho-mimetic variant of this ‘EVO patch’ or a negatively charged peptide is sufficient to diminish assembly formation, suggesting that hijacking mechanisms governing solubility of glutamine-rich TFs may offer new strategies for treatment of polyQ expansion diseases.
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Project description:References:
1. Xiaomei Zhu, Lan Yin, Leroy Hood, David Galas and Ping Ao, Efficiency, Robustness and Stochasticity of Gene Regulatory networks in Systems biology: Lambda switch as a working example, 2006.
2. Adam Arkin, John Ross and Harley H. McAdams, Stochastic kinetic analysis of developmental pathway bifurcation in phage lambda-infected Escherichia coli cells, 1998, Genetics, 149: 1633-1648.
3. GenBank sequence: NC_001416 is the whole genome sequence of phage lambda.
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Project description:Introduction: Lambda interferons signal through the interferon lambda receptor-1 (IFNLR1) and IL10RB heterodimer to induce interferon stimulated genes (ISGs). We previously showed that proteins derived from distinct IFNLR1 splice isoforms uniquely influence gene expression and HBV replication in stem cell-derived hepatocytes (iHeps). Here, we evaluated the mechanisms of signal transduction by full-length IFNLR1 (variant 1) and a truncated variant missing part of the cytoplasmic JAK1-interacting domain (variant 2). Methods: We evaluated HEK293T cells, wild-type (WT), and IFNLR1 knock-out (KO) iHeps with doxycycline-inducible expression FLAG-tagged IFNLR1 variants using the Duolink proximity ligation assay, ImageStream flow cytometry, western blotting of JAK-STAT proteins, susceptibility to JAK1 and TYK2 inhibitors, and gene expression profiling. Results: Each variant demonstrated IFNL-induced colocalization with IL10RB, but variant 1 was more rapidly and extensively internalized. In WT iHeps with intact endogenous IFNLR1, overexpression of either variant 1 or variant 2 enabled higher IFNL-induced JAK1, TYK2, STAT1 and STAT2 phosphorylation, yet variant 2 supported less robust ISG induction than variant 1. In iHeps with abrogated endogenous IFNLR1 expression, variant 2 supported less JAK1 and TYK2 phosphorylation and ISG induction than variant 1 yet was not deficient in supporting STAT1 and STAT2 phosphorylation. Select ISGs had differential constitutive expression in IFNL-untreated variant-expressing iHeps. In iHeps expressing variant 1, WT-iHeps were more resistant than KO-iHeps to TYK2-inhibition of antiviral ISG induction yet conversely were more susceptible to TYK2-inhibition of proinflammatory ISG induction, suggesting endogenously produced noncanonical variants influence the TYK2-dependence of IFNL signaling. Conclusions: IFNLR1 variants promote differential utilization of signaling mediators to influence IFNL-induced gene expression patterns, indicating a putative role in pathway regulation.
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Project description:The Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has had devastating impacts on our global society. Although vaccines and monoclonal antibody countermeasures have reduced the morbidity and mortality associated with SARS-CoV-2 infection, variants with constellations of mutations in the spike gene threaten their efficacy. Therefore, antiviral interventions that are resistant to further virus evolution may be needed. Here, we show IFN-λ protects against SARS-CoV-2 B.1.351 (Beta) and B.1.1529 (Omicron) variants in three strains of conventional and human ACE2 transgenic mice. Prophylaxis or therapy with nasally-delivered IFN-λ2 limited infection of historical or variant (B.1.351 and B.1.1.529) SARS-CoV-2 strains in both the upper and lower respiratory tracts without causing excessive inflammation. In the lung, IFN-λ was produced preferentially in epithelial cells and acted on radio-resistant cells to protect against of SARS-CoV-2 infection. Thus, inhaled IFN-λ may have promise as a treatment for evolving SARS-CoV-2 variants that develop resistance to antibody-based countermeasures.
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