Ontology highlight
ABSTRACT:
PROVIDER: PRJNA575066 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10208140_1.fastq.gz | Fastqsanger.gz | |||
| SRR10208140_2.fastq.gz | Fastqsanger.gz | |||
| SRR10208141_1.fastq.gz | Fastqsanger.gz | |||
| SRR10208141_2.fastq.gz | Fastqsanger.gz | |||
| SRR10208142_1.fastq.gz | Fastqsanger.gz |
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Project description:Abnormal DNA sensing mediated by cGAS-STING is pivotal for host defenses. Activation of cGAS-STING triggered interferon dependent anti-viral functions have been well characterized but this function is missing in more ancient animal STING. Whether more primitive animal STING can generate non-canonical pathway dependent anti-viral activities is unclear. Here, we discovered potent anti-viral activities of ancient animal STING in the absence of all three canonical pathways. Various ancient animal STING-stimulated genes (ASGs) with unique and synergistic anti-viral functions were induced by this newly identified pathway through an ancient transcriptional regulator IRF1 and a separate unique functional domain in STING. Some ASGs are both necessary and sufficient as host restriction factors and under positive selection during animal evolution. Diverse viruses have developed strategies to evade this newly identified cGAS-STING function. Our findings reveal an ancient, conserved cGAS-STING pathway mediated anti-viral activities through previously unrecognized cellular restriction factors. Various animal STING expression in HEK293T cells could up regulate a series of genes. To screen candidates for anti-viral host factors stimulated by STING in the absence of the known canonical pathways, we identified the factors that were regulated by the IFN induction and NF-κB induction-defective Nematostella vectensis (N.v) STING and the IFN induction-defective human STING variant (H.s STING ΔCTT) by microarray assay. Multiple rounds of confirmative and comparative experiments narrowed down to 10 such factors, i.e., ancient animal STING stimulated genes (ASGs). ASGs were significantly upregulated by STING activation in various human cell types.
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Project description:All but a few eukaryotes die without oxygen and respond dynamically to changes in the level of oxygen available to them. One ancient oxygen-requiring biochemical pathway in eukaryotes is the pathway for the biosynthesis of sterols, leading to cholesterol in animals and ergosterol in fungi. Mutations in this pathway are a frequent cause of azole drug resistance in pathogenic fungi. The regulatory mechanism for the sterol pathway is also widely conserved between animals and fungi and is centred on a transcription activator, SREBP, that forms part of a sterol-sensing complex. However, in one group of yeasts – the Saccharomycotina, which includes the major pathogen Candida albicans – control of the sterol pathway has been taken over by an unrelated regulatory protein, Upc2. We show here by analysis of the yeast Yarrowia lipolytica that the evolutionary switch from SREBP to Upc2 was a two-step process in which Upc2 appeared in an ancestor of Saccharomycotina, and SREBP subsequently degenerated and lost its sterol-regulatory function while retaining an ancient role in filamentation.
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Project description:The Mediator is composed of multiple of proteins in the head, body, tail and CDK subunits conserved from yeast to humans. However, not all the components are required for transcription. Components of the tail subunit are not essential but to varying degrees are required for changes in transcription to stress. While some stresses are familiar such as heat, desiccation, and starvation, others are exotic yet elicit a physical stress response. MCHM is a hydrotrope that induces growth arrest in yeast. By exploiting genetic variation, specifically in Med15, between yeast strains, we found that Med15 with the polyQ expansion conferred MCHM sensitivity. This sensitivity was not from a loss of function as the reciprocal hemizygous hybrids were all sensitive, suggesting that there is an incompatibility between Mediator complexes from genetic divergent yeast strains. Transcriptomics from yeast expressing the incompatible Med15 changed expression in diverse pathways. Expansion of polyQ tracts in Med15 resulted in multiple isoforms which were mostly from likely post-translational modifications. Stability of Med15 was dependent on Ydj1, a chaperone and the incompatible Med15 allele was expressed at lower levels and less stable than the compatible Med15 allele. Med15 is tethered to the rest of the Mediator complex via Med2 and 3. Deletion of either Med2 or Med3 changes the Med15 isoform patterns in the in a similar manner whereas deletion of Med5, a distal component of the tail did not change the pattern. The med2 and 3 mutants are similarly sensitive to MCHM while med5 mutants are not. Differences between the Med15 alleles extend to responses to different stresses. Whereas the incompatible allele of Med15 improved growth to chemicals that produce free radicals, and the compatible allele of Med15 improved growth to reducing agents, caffeine, and hydroxyurea. This may reflect the positive and negative role that Med15 has in transcription.
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