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Phage Phenomics: Physiological Approaches to Characterize Novel Viral Proteins
Published on: June 11, 2015
Viral Satellites Exploit Phage Proteins to Escape Degradation of the Bacterial Host Chromosome
Amelia C McKitterick1, Stephanie G Hays1, Fatema-Tuz Johura2
1Department of Plant and Microbial Biology, University of California, Berkeley, 271 Koshland Hall, Berkeley, CA 94720, USA.
Abstract:
Phage defense systems are often found on mobile genetic elements (MGEs), where they constitutively defend against invaders or are induced to respond to new assaults. Phage satellites, one type of MGE, are induced during phage infection to promote their own transmission, reducing phage production and protecting their hosts in the process. One such satellite in Vibrio cholerae, phage-inducible chromosomal island-like element (PLE), sabotages the lytic phage ICP1, which triggers PLE excision from the bacterial chromosome, replication, and transduction to neighboring cells. Analysis of patient stool samples from different geographic regions revealed that ICP1 has evolved to possess one of two syntenic loci encoding an SF1B-type helicase, either of which PLE exploits to drive replication. Further, loss of PLE mobilization limits anti-phage activity because of phage-mediated degradation of the bacterial genome. Our work provides insight into the unique challenges facing parasites of lytic phages and underscores the adaptions of satellites to their ever-evolving target phage.
Insights
Phage satellites like Vibrio cholerae
Area of Science:
- Microbiology
- Molecular Biology
- Genetics
Background:
- Mobile genetic elements (MGEs) harbor phage defense systems.
- Phage satellites are MGEs that propagate by hijacking phage replication cycles.
- Vibrio cholerae possesses a phage satellite, PLE, that targets the lytic phage ICP1.
Purpose of the Study:
- To investigate the co-evolutionary dynamics between the Vibrio cholerae phage satellite PLE and its target phage ICP1.
- To understand how PLE exploits ICP1's genetic elements for its own replication and transmission.
- To elucidate the mechanisms of phage defense and counter-defense in this system.
Main Methods:
- Genomic analysis of Vibrio cholerae and ICP1 isolates.
- Experimental manipulation of PLE and ICP1 interactions.
- Phage-mediated bacterial genome degradation assays.
Main Results:
- ICP1 has evolved two distinct loci encoding SF1B-type helicases, both utilized by PLE for replication.
- PLE's mobilization is crucial for its anti-phage activity, as its loss leads to phage-mediated bacterial genome degradation.
- PLE effectively sabotages ICP1 replication, reducing phage production and protecting the host bacterium.
Conclusions:
- PLE demonstrates remarkable adaptation to its target phage ICP1, exploiting specific genetic loci for its propagation.
- The co-evolutionary arms race between phage and satellite involves intricate molecular mechanisms and genetic adaptations.
- Understanding these interactions provides insights into phage-host dynamics and the evolution of mobile genetic elements.
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