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    Mitochondrial UPR repression during Pseudomonas aeruginosa infection requires the bZIP protein ZIP-3

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    Authors
    Deng, Pan
    Uma Naresh, Nandhitha
    Du, Yunguang
    Lamech, Lilian T.
    Yu, Jun
    Zhu, Lihua Julie
    Pukkila-Worley, Read
    Haynes, Cole M.
    UMass Chan Affiliations
    Department of Molecular, Cell and Cancer Biology
    Department of Medicine, Division of Infectious Diseases and Immunology
    Document Type
    Journal Article
    Publication Date
    2019-03-26
    Keywords
    mitochondrial UPR
    ZIP-3
    ATFS-1
    UPRmt
    immunity
    Cell Biology
    Immunology and Infectious Disease
    Infectious Disease
    Microbiology
    
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    Link to Full Text
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6442607/
    Abstract
    Mitochondria generate most cellular energy and are targeted by multiple pathogens during infection. In turn, metazoans employ surveillance mechanisms such as the mitochondrial unfolded protein response (UPR(mt)) to detect and respond to mitochondrial dysfunction as an indicator of infection. The UPR(mt) is an adaptive transcriptional program regulated by the transcription factor ATFS-1, which induces genes that promote mitochondrial recovery and innate immunity. The bacterial pathogen Pseudomonas aeruginosa produces toxins that disrupt oxidative phosphorylation (OXPHOS), resulting in UPR(mt) activation. Here, we demonstrate that Pseudomonas aeruginosa exploits an intrinsic negative regulatory mechanism mediated by the Caenorhabditis elegans bZIP protein ZIP-3 to repress UPR(mt) activation. Strikingly, worms lacking zip-3 were impervious to Pseudomonas aeruginosa-mediated UPR(mt) repression and resistant to infection. Pathogen-secreted phenazines perturbed mitochondrial function and were the primary cause of UPR(mt) activation, consistent with these molecules being electron shuttles and virulence determinants. Surprisingly, Pseudomonas aeruginosa unable to produce phenazines and thus elicit UPR(mt) activation were hypertoxic in zip-3-deletion worms. These data emphasize the significance of virulence-mediated UPR(mt) repression and the potency of the UPR(mt) as an antibacterial response.
    Source

    Deng P, Uma Naresh N, Du Y, Lamech LT, Yu J, Zhu LJ, Pukkila-Worley R, Haynes CM. Mitochondrial UPR repression during Pseudomonas aeruginosa infection requires the bZIP protein ZIP-3. Proc Natl Acad Sci U S A. 2019 Mar 26;116(13):6146-6151. doi: 10.1073/pnas.1817259116. Epub 2019 Mar 8. PMID: 30850535; PMCID: PMC6442607. Link to article on publisher's site

    DOI
    10.1073/pnas.1817259116
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/35189
    PubMed ID
    30850535
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    Link to Article in PubMed

    ae974a485f413a2113503eed53cd6c53
    10.1073/pnas.1817259116
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