ArticleNature microbiology2025
Host AAA-ATPase VCP/p97 lyses ubiquitinated intracellular bacteria as an innate antimicrobial defence.
Article in Nature microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Cell-autonomous immunity as an integrated immune network against bacterial and viral pathogens.Nature microbiology · 2026Review
- Cytosolic CTH senses bacterial lipoproteins and drives noncanonical inflammasome activation.Nature immunology · 2026Article
- Enzymatic cleavage weaponizes bacterial lipoproteins into immune tripwires.Nature immunology · 2026Article
- Manipulation of nonclassical ubiquitin signaling by pathogenic bacteria.Current opinion in microbiology · 2026Review
- The active secretion of a subunit of IL-12 by tissue cells is regulated by Valosin-Containing Protein and intracellular calcium redistribution.bioRxiv : the preprint server for biology · 2026Article
- A diverse family of bacterial deubiquitinases is defined by theProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Extract to lyse bacterial pathogens.Nature microbiology · 2025Article
Corrections and comments
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Authors and funding
18 authors.
Funding
Abstract
Cell-autonomous immunity prevents intracellular pathogen growth through mechanisms such as ubiquitination and proteasomal targeting of bacteria for degradation. However, how the proteasome eradicates ubiquitinated bacteria has remained unclear. Here we show that host AAA-ATPase, VCP/p97, associates with diverse cytosol-exposed ubiquitinated bacteria (Streptococcus pneumoniae, Salmonella enterica serovar Typhimurium, Streptococcus pyogenes) and requires the ATPase activity in its D2 domain to reduce intracellular bacterial loads. Combining optical trap approaches along with molecular dynamic simulations, in vitro reconstitution and immunogold transmission electron microscopy, we demonstrate that p97 applies mechanical force to extract ubiquitinated surface proteins, BgaA and PspA, from S. pneumoniae cell membranes. This causes extensive membrane lysis and release of cytosolic content, thereby killing the pathogen. Further, p97 also controls S. pneumoniae proliferation in mice, ultimately protecting from fatal sepsis. Overall, we discovered a distinct innate antimicrobial function of p97 that can protect the host against lethal bacterial infections.
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Registered trials
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