Antibiotics stimulate protein transfer to persister cells

• 成果类型: Article
• 署名作者: Wen, Alice X.; Bos, Julia; Panda, Debojyoti; Hagstrom, Katelin M.; Singh, Shubham; Mageswaran, Shrawan Kumar; Wang, Xiaoli; Hu, Bo; Welch, Kobie T.; Cooke, Matthew B.; Halliday, Jennifer A.; Ramirez, Laura Deus; Martinez, Antoinette E.; Chang, Yi-Wei; Weitz, David A.; Herman, Christophe
• 署名单位: Baylor College of Medicine; Baylor College of Medicine; Centre National de la Recherche Scientifique (CNRS); Universite Paris Cite; Pasteur Network; Institut Pasteur Paris; CNRS - National Institute for Biology (INSB); Harvard University; Baylor College of Medicine; Baylor College of Medicine; Baylor College of Medicine; University of Pennsylvania; Pennsylvania Medicine; Baylor College of Medicine; University of Texas System; University of Texas Health Science Center Houston; University of Pennsylvania; Pennsylvania Medicine; Harvard University; Harvard University; Baylor College of Medicine; Baylor College of Medicine
• 刊物名称: SCIENCE
• ISSN/ISSBN: 0036-8075; 1095-9203
• DOI: 10.1126/science.adx3972
• 发表日期: 2026-06-25
• 页码: eadx3972
• 关键词: outer-membrane vesicles; escherichia-coli; VIRULENCE GENES; PSP RESPONSE; bacteria; stress; quantification; phospholipids; Visualization; GROWTH

摘要

The exchange of biological matter between bacterial cells drives adaptation and evolution. However, whether bacteria can exchange functional proteins remains unclear. In this work, we found that antibiotic treatment can induce vesicle-mediated horizontal protein transfer within and between bacterial species. We developed a genetic system in Escherichia coli to track transfer events and performed single-cell transcriptomic profiling on an isogenic population of bacteria. Antibiotics stimulated the differentiation of this isogenic population into distinct cell states: donor cells that activated a membrane stress response to release protein-containing vesicles and recipient cells that suppressed this response to acquire protein from their neighbors. Protein uptake enhanced the antibiotic persistence of recipient cells, revealing that vesicle exchange promotes bacterial survival during antibiotic treatment.