أعرض في EDS

Enterococcal quorum-controlled protease alters phage infection.

التفاصيل البيبلوغرافية
العنوان: Enterococcal quorum-controlled protease alters phage infection.
المؤلفون: Sheriff EK; Department of Immunology and Microbiology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045., Salvato F; Department of Plant and Microbial Biology, North Carolina State University, Raleigh, NC 27695., Andersen SE; Department of Immunology and Microbiology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045., Chatterjee A; Department of Immunology and Microbiology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045., Kleiner M; Department of Plant and Microbial Biology, North Carolina State University, Raleigh, NC 27695., Duerkop BA; Department of Immunology and Microbiology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045.
المصدر: BioRxiv : the preprint server for biology [bioRxiv] 2024 May 11. Date of Electronic Publication: 2024 May 11.
نوع المنشور: Preprint
اللغة: English
بيانات الدورية: Country of Publication: United States NLM ID: 101680187 Publication Model: Electronic Cited Medium: Internet ISSN: 2692-8205 (Electronic) Linking ISSN: 26928205 NLM ISO Abbreviation: bioRxiv Subsets: PubMed not MEDLINE
مستخلص: Increased prevalence of multidrug resistant bacterial infections has sparked interest in alternative antimicrobials, including bacteriophages (phages). Limited understanding of the phage infection process hampers our ability to utilize phages to their full therapeutic potential. To understand phage infection dynamics we performed proteomics on Enterococcus faecalis infected with the phage VPE25. We discovered numerous uncharacterized phage proteins are produced during phage infection of Enterococcus faecalis . Additionally, we identified hundreds of changes in bacterial protein abundances during infection. One such protein, enterococcal gelatinase (GelE), an fsr quorum sensing regulated protease involved in biofilm formation and virulence, was reduced during VPE25 infection. Plaque assays showed that mutation of either the fsrA or gelE resulted in plaques with a "halo" morphology and significantly larger diameters, suggesting decreased protection from phage infection. GelE-associated protection during phage infection is dependent on the murein hydrolase regulator LrgA and antiholin-like protein LrgB, whose expression have been shown to be regulated by GelE. Our work may be leveraged in the development of phage therapies that can modulate the production of GelE thereby altering biofilm formation and decreasing E. faecalis virulence.
التعليقات: Update in: FEMS Microbes. 2024 Jul 26;5:xtae022. doi: 10.1093/femsmc/xtae022. (PMID: 39156124)
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معلومات مُعتمدة: R01 AI141479 United States AI NIAID NIH HHS; R35 GM138362 United States GM NIGMS NIH HHS
تواريخ الأحداث: Date Created: 20240520 Latest Revision: 20240827
رمز التحديث: 20240827
مُعرف محوري في PubMed: PMC11100838
DOI: 10.1101/2024.05.10.593607
PMID: 38766208
قاعدة البيانات: MEDLINE
الوصف
تدمد:2692-8205
DOI:10.1101/2024.05.10.593607