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The PDIM paradox of Mycobacterium tuberculosis: new solutions to a persistent problem

Claire V Mulholland1, Thomas J Wiggins1, Jinhua Cui1

  • 1Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York, USA.

Biorxiv : the Preprint Server for Biology
|October 31, 2023
PubMed

Insights

Phthiocerol dimycocerosate (PDIM) loss in Mycobacterium tuberculosis is caused by methylmalonyl-CoA deficiency. Supplementing with odd-chain fatty acids or vitamin B12 can restore PDIM production and virulence.

Area of Science:

  • Microbiology
  • Biochemistry

Background:

  • Phthiocerol dimycocerosate (PDIM) is a crucial virulence lipid in *Mycobacterium tuberculosis*.
  • Spontaneous mutations during *in vitro* culture lead to PDIM loss, resulting in attenuated virulence and increased cell wall permeability.

Approach:

  • Investigated the metabolic basis of PDIM loss, identifying a methylmalonyl-CoA deficiency.
  • Developed a scalable assay to measure PDIM production.
  • Tested supplementation strategies including odd-chain fatty acids, cholesterol, and vitamin B12.

Key Points:

  • PDIM loss stems from a metabolic bottleneck in methylmalonyl-CoA synthesis.
  • Supplementation with specific nutrients (odd-chain fatty acids, cholesterol, vitamin B12) can restore PDIM production.
  • Propionate supplementation enhances PDIM-producing *M. tuberculosis* growth and selects against PDIM-negative mutants.

Conclusions:

  • The study resolves a significant challenge in tuberculosis research by elucidating the cause of PDIM loss during *in vitro* culture.
  • Demonstrates how nutrient environment differences between host and *in vitro* settings impact bacterial pathogenicity.
  • Highlights the potential for nutrient manipulation to control *M. tuberculosis* virulence.

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