ArticleNature communications2024
The double-edged role of FASII regulator FabT in Streptococcus pyogenes infection.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- Monounsaturated fatty acid biosynthesis is critical for streptococcal envelope homeostasis and stress tolerance.Journal of bacteriology · 2026Article
- Carbon metabolism and niche adaptation inmSphere · 2026Review
- Article
- Monounsaturated fatty acid biosynthesis is critical for streptococcal envelope homeostasis and stress tolerance.bioRxiv : the preprint server for biology · 2026Article
- Article
- Oxidative stress is intrinsic to staphylococcal adaptation to fatty acid synthesis antibiotics.iScience · 2024Article
- Acyl-AcpB, a FabT corepressor inJournal of bacteriology · 2023Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
In Streptococcus pyogenes, the type II fatty acid (FA) synthesis pathway FASII is feedback-controlled by the FabT repressor bound to an acyl-Acyl carrier protein. Although FabT defects confer reduced virulence in animal models, spontaneous fabT mutants arise in vivo. We resolved this paradox by characterizing the conditions and mechanisms requiring FabT activity, and those promoting fabT mutant emergence. The fabT defect leads to energy dissipation, limiting mutant growth on human tissue products, which explains the FabT requirement during infection. Conversely, emerging fabT mutants show superior growth in biotopes rich in saturated FAs, where continued FASII activity limits their incorporation. We propose that membrane alterations and continued FASII synthesis are the primary causes for increased fabT mutant mortality in nutrient-limited biotopes, by failing to stop metabolic consumption. Our findings elucidate the rationale for emerging fabT mutants that improve bacterial survival in lipid-rich biotopes, but lead to a genetic impasse for infection.
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