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NCoR1: a key player regulating mycobacterium tuberculosis pathogenesis.

Kaushik Sen1,2, Viplov Kumar Biswas1,3, Arup Ghosh1,3

  • 1Immuno-genomics & Systems Biology Laboratory, Institute of Life Sciences (ILS), Bhubaneswar, Odisha, India.

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Summary
This summary is machine-generated.

NCOR1 depletion impairs host defense against Mycobacterium tuberculosis (Mtb) by disrupting autophagy and lysosome function via the AMPK-MTOR-TFEB pathway. Restoring NCOR1 or using specific treatments can enhance Mtb clearance.

Keywords:
AMPKMTORNCOR1TFEBmycobacterium tuberculosis

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Area of Science:

  • Cellular Biology
  • Immunology
  • Microbiology

Background:

  • Mycobacterium tuberculosis (Mtb) evades host defenses, including autophagy and lysosome function.
  • NCOR1, a transcriptional co-repressor, is implicated in various cellular processes but its role in Mtb pathogenesis is unknown.

Purpose of the Study:

  • To investigate the role of NCOR1 in regulating autophagy, lysosome biogenesis, and Mtb pathogenesis.
  • To explore the therapeutic potential of targeting NCOR1 in host-directed therapies against Mtb.

Main Methods:

  • Depletion of NCOR1 in host cells.
  • Analysis of the AMPK-MTOR-TFEB signaling axis and its impact on autophagy and lysosome biogenesis.
  • Treatment of NCOR1-depleted cells with rapamycin, antimycin A, or metformin.
  • Assessment of Mtb survival and clearance in host cells.

Main Results:

  • NCOR1 depletion disrupts the AMPK-MTOR-TFEB pathway, impairing autophagy and lysosome biogenesis, leading to increased Mtb survival.
  • Restoration of TFEB activity and autophagic flux (LC3-II levels) was achieved by treating NCOR1-depleted cells with rapamycin, antimycin A, or metformin.
  • Exogenous NCOR1 expression rescued the signaling axis and autophagic machinery.

Conclusions:

  • NCOR1 plays a critical role in host defense against Mtb by regulating autophagy and lysosome function.
  • Targeting NCOR1 or modulating the AMPK-MTOR-TFEB pathway presents a promising strategy for novel host-directed therapies against tuberculosis.