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Updated: Feb 10, 2026

Deciphering and Imaging Pathogenesis and Cording of Mycobacterium abscessus in Zebrafish Embryos
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Deciphering and Imaging Pathogenesis and Cording of Mycobacterium abscessus in Zebrafish Embryos

Published on: September 9, 2015

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A highly conserved two-gene operon is crucial for lipoarabinomannan localization, pathogenesis, and cell envelope

Nicholas Campbell-Kruger1, Amir Balakhmet1, Sarah A Stanley1

  • 1Division of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, USA.

Biorxiv : the Preprint Server for Biology
|February 9, 2026
PubMed

Insights

The lprg-mfs operon is crucial for Mycobacterium abscessus virulence and its cell envelope integrity. This study reveals its role in lipoarabinomannan transport, impacting antibiotic resistance.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Pathogenesis

Background:

  • Mycobacterium abscessus infections are difficult to treat due to antibiotic resistance.
  • The determinants of M. abscessus virulence and physiology are not well understood.
  • The lprg-mfs operon's function in M. abscessus remains unclear.

Purpose of the Study:

  • To investigate the role of the lprg-mfs operon in M. abscessus virulence and cell envelope homeostasis.
  • To understand the mechanism of lipoarabinomannan (LAM) distribution in M. abscessus.
  • To identify factors regulating mycomembrane properties.

Main Methods:

  • Genetic manipulation of the lprg-mfs operon in M. abscessus.
  • Assessment of virulence in macrophage and mouse models.
  • Analysis of lipoarabinomannan (LAM) localization and cell envelope characteristics (permeability, fluidity, integrity).
  • Suppressor screening to identify complementary genes.

Main Results:

  • The lprg-mfs operon is essential for M. abscessus virulence in macrophages and mice.
  • Loss of lprg-mfs leads to LAM accumulation on the cell surface and in supernatant, suggesting a role in LAM import.
  • The lprg-mfs mutant exhibits defects in mycomembrane permeability, fluidity, and integrity.
  • A mutation in MAB_0995 can complement the lprg-mfs deletion phenotypes.
  • LAM regulation in the mycomembrane is dynamic and responsive to environmental conditions.

Conclusions:

  • The lprg-mfs operon plays a critical role in M. abscessus pathogenesis and cell envelope homeostasis.
  • This study redefines the function of LprG/Mfs in mycobacterial lipid transport, contrasting with M. tuberculosis.
  • Mycomembrane lipid regulation in M. abscessus is more plastic than previously thought.

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