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Congratulations to Yuzhe Weng, a DPhil student in the Platt lab, who is first author on new paper published by the group in Nature Communications. Mycobacteria tuberculosis (Mtb), the causative agent of tuberculosis (TB), has the ability to invade, persist and replicate within host cells, which is key to its success as a pathogen. However, the mechanisms that underlie this strategy remain poorly defined.

Previous research in the Platt lab demonstrated the unexpected phenotypic similarity of cells infected with pathogenic mycobacteria and cells from the rare lysosomal storage disorder Niemann-Pick type C disease (NPC) in which the activity of the lysosomal protein NPC1 is impaired. The lab found that Mtb sheds cell wall lipids that inhibit NPC1 and as a consequence induce cell biological changes that promote intracellular survival. 

In this new study recently published in Nature Communications, in collaboration with Dr Gerald Larrouy-Maumus and Dr Brian Robertson from Imperial College London, the group has now shown that the ability to inhibit NPC1 and induce NPC cellular phenotypes is widespread amongst global clinical strains of Mtb, other members of the tubercular mycobacteria complex (including M. bovis and M. avium), as well as several species of non-tubercular mycobacteria. However, activity was absent from M. canettii, a mycobacterium that is considered to resemble the common ancestor species, indicating that the ability to inhibit NPC1 evolved early but post divergence from M. canettii-like mycobacteria. These data are consistent with inhibition of NPC1 being an important step in the evolution of pathogenicity by mycobacteria.

See the full paper at:

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