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A mitochondrial quality control mechanism reverses the phagosome maturation arrest caused by Mycobacterium

Surbhi Verma, Mrinmoy Das, Raman D Sharma

    Biorxiv : the Preprint Server for Biology
    |December 11, 2023
    PubMed

    Insights

    Depleting p62 protein disrupts mitochondrial quality control, leading to enhanced targeting of Mycobacterium tuberculosis to lysosomes. This unexpected crosstalk reverses phagosome maturation arrest, offering a new avenue for tuberculosis therapies.

    Area of Science:

    • Cell Biology
    • Immunology
    • Microbiology

    Background:

    • Mycobacterium tuberculosis (Mtb) evades host defenses by arresting phagosome maturation.
    • RAB7 exclusion from Mtb-containing phagosomes is a hallmark of this arrest.

    Conclusions:

    • A novel crosstalk between MQC and phagosome maturation pathways reverses Mtb-induced PMA.
    • p62-dependent MQC pathways, particularly TOM20+ MDVs, are crucial for controlling Mtb infection.
    • Exploiting this MQC-antibacterial pathway offers potential for host-directed anti-tuberculosis therapies.

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