Uncovering bacterial-phage interplay by monitoring transcriptomic changes during phage infection.

• Grant number: 24/01159-8
• Support Opportunities: Scholarships in Brazil - Master
• Start date: March 01, 2024
• End date: February 28, 2026
• Field of knowledge: Biological Sciences - Microbiology - Biology and Physiology of Microorganisms
• Principal Investigator: João Carlos Setubal
• Grantee: Guilherme Wenceslau de Lima Cardoso
• Host Institution: Instituto de Química (IQ). Universidade de São Paulo (USP). São Paulo , SP, Brazil
• Associated research grant: 21/10577-0 - Biology of Bacteria and Bacteriophages Research Center, AP.CEPID

Abstract

Bacterial predation by phages drives an ongoing phage-host arms race. While bacteria defend themselves against phage predation with a large repertoire of defense systems, phages evolve strategies crucial for their successful infection and propagation. Understanding these interactions can reveal how phage modulates bacterial metabolism and inhibits bacterial defense mechanisms to establish an effective infection and is also important for the successful development of phage-based applications. Among the approaches employed to discover of mechanisms of phage-host interaction, transcriptomic analysis using RNA sequencing (RNA-seq) has proven a valuable tool to study phage and bacteria gene expression profile during the infection. This project aims to investigate phage-host interactions along the infection cycle of Pseudomonas aeruginosa PA14 with phages ZC01 (Siphoviridae; Abidjanvirus; unclassified Abidjanvirus) and ZC03 (Schitoviridae; Zicotriavirus; Pseudomonas virus ZC03) which we have previously isolated and characterized. These are genomically and morphologically unrelated phages that infect the same bacterial host strain and show narrow host range (at strain level). Our unpublished results suggest type-4 pilus pilin (PilA) as the primary determinant for ZC01 while ZC03 seems to depend on both LPS and PilA for specific adsorption. P. aeruginosa PA14 cultures will be infected with ZC01 and/or ZC03 and transcriptional changes in the bacterial host will be accessed from early to late times of the lytic infection. The transcriptional changes of PA14 infected with ZC01 and/or ZC03 will be accessed under in vitro conditions where this bacterial strain exhibits virulence-related phenotype.