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    Home > Biochemistry News > Microbiology News > The team of Wang Linqi of the Institute of Microbiology reveals the formation mechanism of the antiviral morphology of fungi induced by the dietary supplement "Gugli"

    The team of Wang Linqi of the Institute of Microbiology reveals the formation mechanism of the antiviral morphology of fungi induced by the dietary supplement "Gugli"

    • Last Update: 2021-11-13
    • Source: Internet
    • Author: User
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    The conversion between yeast and hyphae is a unique biological process of fungi, which generally determines the pathogenicity of pathogenic fungi
    .

    For example, among the pathogenic fungi of the genus Cryptococcus with a high lethality rate (the annual lethality is about 200,000; the lethality rate is> 20%), the yeast form is a highly virulent form, while the mycelial form is not pathogenic and can stimulate the host to produce immunity Protection is called anti-virulence morphotype
    .

     ● ● ●Recently, the international journal PLoS Genetics published online the research results of Wang Linqi's team at the State Key Laboratory of Mycology, Institute of Microbiology, Chinese Academy of Sciences, "A unique cell wall synthetic response evoked by glucosamine determines pathogenicity-associated fungal cellular differentiation"
    .

    This study reveals the molecular/cellular mechanism of the extremely safe glucosamine (the main component of dietary supplement "Guli") inducing the formation of cryptococcal antivirulence, implying that it can be used as a new anti-infective drug and for other pathogenic fungi The development of anti-infection strategies provides a new perspective
    .

     Figure 1 Phenotypic group association analysis combined with multi-time point gene expression feature analysis to identify the key biological processes induced by glucosamine.
    Researchers first used phenotype group association analysis combined with multi-time point gene expression feature analysis to find that glucosamine stimulates the global cell wall In response to the response, the formation of antiviral hyphae is induced
    .

    Glucosamine induces the continuous synthesis of the cell wall, which in turn drives the formation of antiviral hyphae (Figure 1)
    .

    In this process, the cell surface protein Gis1 can be used as a molecular pointer to specifically indicate the global cell wall synthesis response stimulated by glucosamine (Figure 2)
    .

    Figure 2 The cell surface protein Gis1 is used as a molecular marker to specifically indicate the global cell wall synthesis response induced by glucosamine.
    The researchers then discovered that the Mpk1 cell wall integrity pathway is the core pathway that controls the morphology of antiviral hyphae induced by glucosamine
    .

    Through phosphoproteome combined with functional genomics methods, the downstream regulators of Mpk1 kinase, Skn7 and Crz1, were identified as the core components of this pathway to control the formation of antiviral hyphae (Figure 3)
    .

     Figure 3 Phosphoproteomics combined with functional genomics analysis to identify the core target protein of Mpk1.
    This research has won the National Key Research and Development Program (2021YFC2100600), the National Natural Science Foundation of China (31770163, 31622004, 31970077), and the Chinese Academy of Sciences Key Research Program (QYZDB-SSW) -SSMC040), the National Science and Technology Major Project (2018ZX10101004) and the Chinese Academy of Sciences' Science and Technology Innovation "Cross and Cooperation Team" and other funds
    .

    Special research assistant Dr.
    Hu Pengjie, PhD student Ding Hao, and assistant researcher Shen Lan (currently working unit Chongqing Meiled Biomedical Co.
    , Ltd.
    ) are the co-first authors of the paper
    .

    Researcher Yang Ence of Peking University Health Science Center, Professor Xu Xinping of the First Affiliated Hospital of Nanchang University, and Jincheng researcher team of Institute of Microbiology of Chinese Academy of Sciences are important collaborators in this research
    .

    Link to the original text: https://journals.
    plos.
    org/plosgenetics/article?id=10.
    1371/journal.
    pgen.
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