Presentation Type
Poster Presentation
Category
STEM (science, technology, engineering, mathematics)
Abstract/Artist Statement
The causative agent of Lyme disease in North America, Borrelia (Borreliella) burgdorferi (Bb), is maintained in an enzootic cycle between a tick vector and non-human vertebrate hosts. Persistence within these host populations requires both immune evasion and genetic diversity, yet the mechanisms contributing to diversity in Bb remain understudied. One potential contributor to Bb genetic diversity is fBB-1, a bacteriophage that packages the ubiquitous 32-kb circular plasmid (cp32) family via a headful mechanism. The cp32 plasmids encode variable outer surface lipoproteins implicated in antigenic variation.
We hypothesize that fBB-1 contributes to Bb genetic diversity via transduction of the cp32s, facilitating reinfection within host reservoir populations. The nucleic acid–binding protein BpuR binds to the pac site of cp32 prophages, suggesting a role in regulating phage packaging and, by extension, cp32 production.
The purpose of this study was to determine the role of BpuR in fBB-1 phage production and to explore its potential involvement in coordinating bacteriophage activity with host-adaptive gene regulation in Bb.
To address this, we generated a bpuR null mutant and complement. Bacteriophage production was increased in the bpuRmutant via as assayed by immunoblotting of the major capsid protein and qPCR of the cp32 prophage. These data demonstrate that BpuR functions as a negative regulator of phage production. In addition, analysis of Bb proteins in the bpuR mutant revealed increased levels of RpoS, the alternative sigma factor that controls the regulon required for vertebrate host infection.
These findings suggest that BpuR may serve as one of the first mechanistic bridges between RpoS-mediated regulation of vertebrate infection and bacteriophage-driven genetic diversity. Together, these data support a model in which BpuR coordinates phage production and host-adaptive gene expression, contributing to the maintenance of Bb within its enzootic cycle.
Mentor Name
Scott Samuels
BpuR Regulates Bacteriophage Production and Gene Expression in the Lyme Disease Spirochete
UC North Ballroom
The causative agent of Lyme disease in North America, Borrelia (Borreliella) burgdorferi (Bb), is maintained in an enzootic cycle between a tick vector and non-human vertebrate hosts. Persistence within these host populations requires both immune evasion and genetic diversity, yet the mechanisms contributing to diversity in Bb remain understudied. One potential contributor to Bb genetic diversity is fBB-1, a bacteriophage that packages the ubiquitous 32-kb circular plasmid (cp32) family via a headful mechanism. The cp32 plasmids encode variable outer surface lipoproteins implicated in antigenic variation.
We hypothesize that fBB-1 contributes to Bb genetic diversity via transduction of the cp32s, facilitating reinfection within host reservoir populations. The nucleic acid–binding protein BpuR binds to the pac site of cp32 prophages, suggesting a role in regulating phage packaging and, by extension, cp32 production.
The purpose of this study was to determine the role of BpuR in fBB-1 phage production and to explore its potential involvement in coordinating bacteriophage activity with host-adaptive gene regulation in Bb.
To address this, we generated a bpuR null mutant and complement. Bacteriophage production was increased in the bpuRmutant via as assayed by immunoblotting of the major capsid protein and qPCR of the cp32 prophage. These data demonstrate that BpuR functions as a negative regulator of phage production. In addition, analysis of Bb proteins in the bpuR mutant revealed increased levels of RpoS, the alternative sigma factor that controls the regulon required for vertebrate host infection.
These findings suggest that BpuR may serve as one of the first mechanistic bridges between RpoS-mediated regulation of vertebrate infection and bacteriophage-driven genetic diversity. Together, these data support a model in which BpuR coordinates phage production and host-adaptive gene expression, contributing to the maintenance of Bb within its enzootic cycle.