ArticleCommunications biology2025
ACA kills Mycobacterium tuberculosis and M. bovis by targeting cell wall core assembling protein CpsA.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- Epidemiological investigation ofOpen veterinary journal · 2026Article
- Breaking the barrier: from biosynthetic inhibition to multidimensional modulation of the mycobacterial cell wall in tuberculosis therapy.Frontiers in pharmacology · 2026Review
- The AcasR-FadD9 regulatory axis modulates iron homeostasis and susceptibility to the anti-mycobacterial compound ACA.Frontiers in tuberculosis · 2026Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tuberculosis (TB), caused by Mycobacterium tuberculosis, still globally threatens human health. With the emergence of multidrug-resistant strains, there is an imperative need to discover new anti-TB agents and identify novel drug targets. Here, we report that the compound ACA, namely 3-azidothiophene-2-carboxylic acid, can kill M. tuberculosis by targeting the bacterial cell wall core assembling process. Whole-genome sequencing of spontaneous ACA-resistant mutants identified single-nucleotide variants in the cpsA2 ligase gene responsible for the covalent attachment of arabinogalactan and peptidoglycan. The cell wall of cpsA2 or its homolog cpsA1-deleted mutant H37Ra strains show increased permeability and drug sensitivity, which is similar to the ACA-treated mycobacteria. Both cpsA1 and cpsA2 could reverse the resistant phenotype of ACA-resistant mutants and the growth defects of the ΔcpsA1 H37Ra strain. ACA can directly bind CpsA1 and CpsA2 to inhibit significantly the pyrophosphatase activity of CpsA1 and CpsA2. Our results suggest that ACA may disturb the cell wall core assembling process and kill M. tuberculosis by targeting CpsA1 and CpsA2, which provide potential candidate drug target for controlling drug-resistant TB.
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