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Functional Analysis of Genes in Mycobacterium tuberculosis Action Against Autophagosome–Lysosome Fusion

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Abstract

Tuberculosis is a lethal disease that is one of the world's top ten death-associated infections in humans; Mycobacterium tuberculosis causes tuberculosis, and this bacterium is linked to the lysis of autophagolysosomal fusion action, a self-defense mechanism of its own. Thus, Cytoplasmic bacilli are sequestered by autophagy and transported to lysosomes to be inactivated to destroy intracellular bacteria. Besides this, a macrophage can limit intracellular Mycobacterium by using a type of autophagy, selective autophagy, a cell that marks undesirable ubiquitin existence in cytosolic cargo, acting as a “eat me” sensor in conjunction with cellular homeostasis. Mycobacterium tuberculosis genes of the PE_PGRS protein family inhibit autophagy, increase mycobacterial survival, and lead to latent tuberculosis infection associated with miRNAs. In addition, the family of autophagy-regulated (ATG) gene members are involved in autophagy and controls the initiation, expansion, maturation, and fusion of autophagosomes with lysosomes, among other signaling events that control autophagy flux and reduce inflammatory responses and forward to promote cellular proliferation. In line with the formation of caseous necrosis in macrophages by Mycobacterium tuberculosis and their action on the lysis of autophagosome fusion, it leads to latent tuberculosis infection. Therefore, we aimed to comprehensively analyses the autophagy and self-defense mechanism of Mycobacterium tuberculosis, which is to be gratified future research on novel therapeutic tools and diagnostic markers against tuberculosis.

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  1. Department of Microbiology, SRM Medical College Hospital and Research Centre, Kattangulathur, Chennai, Tamilnadu, 603203, India

    Karthikeyan Sundaram & Leela Kagithakara Vajravelu

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Sundaram, K., Vajravelu, L.K. Functional Analysis of Genes in Mycobacterium tuberculosis Action Against Autophagosome–Lysosome Fusion. Indian J Microbiol (2024). https://doi.org/10.1007/s12088-024-01227-4

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  • DOI: https://doi.org/10.1007/s12088-024-01227-4

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