Year of Award
2022
Document Type
Dissertation
Degree Type
Doctor of Philosophy (PhD)
Degree Name
Cellular, Molecular and Microbial Biology
Department or School/College
Division of Biological Sciences
Committee Chair
Patrick R. Secor
Commitee Members
Michael F. Minnick, Beverly J. Piggott, Brandon S. Cooper, Scott Wetzel, Stephen Lodmell
Keywords
bacteriophage, defense, infection, polyamine
Publisher
University of Montana
Abstract
Cells are constantly monitoring their extracellular environment for danger signals that warn of imminent threats. When cells are killed by physical or other non-infectious injuries, they release concentrated intracellular molecules into the surrounding area. These danger-associated molecules alert other cells that danger is nearby. When cells are killed by pathogens, they release both damage-associated and pathogen-associated signals. Both eukaryotic and bacterial cells sense these molecules and make threat assessments of cellular injury. Here, I show that lysis of Pseudomonas aeruginosa and other bacterial species releases high concentrations of polyamines that are in turn taken up by surviving cells in a process mediated by Gac/Rsm and cyclic-di-GMP signaling. Intracellular polyamine levels spike in neighboring cells, with the duration of the high polyamine levels dictated by the infection status of the cell. In bacteriophage-infected cells, intracellular polyamine levels remain high, resulting in inhibition of bacteriophage genome replication. Linear DNA, whether in the form of packaged bacteriophage DNA or damage-induced linearized host DNA, was sufficient to induce intracellular polyamine accumulation, indicating that linear DNA is interpreted as a secondary danger signal. In addition, we discovered a group of N4-like bacteriophage that have evolved a means to disrupt intracellular polyamine accumulation and to allow for unencumbered phage replication. Because polyamines are ubiquitous to cellular life and Gac/Rsm and cyclic-di-GMP signaling are widespread amongst γ-proteobacteria, we propose that intracellular polyamine accumulation is a general strategy employed by bacteria to defend against bacteriophage infection and allow P. aeruginosa to make threat assessments of cellular injury.
Recommended Citation
de Mattos, Camilia Dornelles, "BACTERIOPHAGE INFECTION INDUCES INTRACELLULAR POLYAMINE ACCUMULATION AS A DEFENSE MECHANISM IN PSEUDOMONAS AERUGINOSA" (2022). Graduate Student Theses, Dissertations, & Professional Papers. 12044.
https://scholarworks.umt.edu/etd/12044
© Copyright 2022 Camilia Dornelles de Mattos