Filamentous cheater phages drive bacterial and phage populations to lower fitness DOI Creative Commons
Nanami Kubota, Michelle R. Scribner, Vaughn S. Cooper

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2025, Volume and Issue: unknown

Published: April 1, 2025

Many bacteria carry phage genome(s) in their chromosome (i.e., prophage), and this intertwines the fitness of bacterium phage. Most Pseudomonas aeruginosa strains filamentous phages called Pf that establish chronic infections do not require host lysis to spread. However, spontaneous mutations repressor gene ( pf5r ) can allow extreme production slows bacterial growth increases cell death, violating an apparent détente between We observed paradoxical outcome evolution experiment with P. media simulating nutrients from cystic fibrosis airway. Bacteria containing mutant grow a lower density but directly outcompete ancestor convert them into mutants via superinfection. Reduced therefore spreads throughout population, driven by weaponized Pf. Yet high intracellular replication facilitates another evolutionary conflict: "cheater miniphages" lacking capsid genes invade populations full-length within cells. Although both miniphages are most immune superinfection limiting receptor, hybrid vigor is extremely unstable, as classic Tragedy Commons scenario ensues results complete prophage loss. The entire cycle - hyperactivation miniphage invasion loss occur 24h, showcasing rapid coevolution phages. This study demonstrates , potentially many other species prophages, risk being exploited these runaway process reduces virus.

Language: Английский

Inovirus-Encoded Peptides Induce Specific Toxicity in Pseudomonas aeruginosa DOI Creative Commons

Juehua Weng,

Yunxue Guo, Jiayu Gu

et al.

Viruses, Journal Year: 2025, Volume and Issue: 17(1), P. 112 - 112

Published: Jan. 15, 2025

Pseudomonas aeruginosa is a common opportunistic pathogen associated with nosocomial infections. The primary treatment for infections typically involves antibiotics, which can lead to the emergence of multidrug-resistant strains. Therefore, there pressing need safe and effective alternative methods. Phage therapy stands out as promising approach. However, filamentous prophages (Pfs) commonly found in P. encode genes phage defense activity, thereby reducing efficacy therapy. Through genomic analysis Pf4 prophage, we identified 102 bp gene co-transcribed upstream responsible release (zot gene), giving rise 33-amino-acid polypeptide that have named Pf4-encoded toxic (PftP4). overexpression PftP4 demonstrated cellular toxicity aeruginosa, subcellular localization indicating its presence cell membrane subsequent increase permeability. Notably, homologues are multiple Pf phages exhibit specificity their towards among tested bacterial Our study reveals novel Pf-encoded has potential selectively target eradicate offering valuable insights combating

Language: Английский

Citations

0
Filamentous cheater phages drive bacterial and phage populations to lower fitness DOI Creative Commons
Nanami Kubota, Michelle R. Scribner, Vaughn S. Cooper

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2025, Volume and Issue: unknown

Published: April 1, 2025

Many bacteria carry phage genome(s) in their chromosome (i.e., prophage), and this intertwines the fitness of bacterium phage. Most Pseudomonas aeruginosa strains filamentous phages called Pf that establish chronic infections do not require host lysis to spread. However, spontaneous mutations repressor gene ( pf5r ) can allow extreme production slows bacterial growth increases cell death, violating an apparent détente between We observed paradoxical outcome evolution experiment with P. media simulating nutrients from cystic fibrosis airway. Bacteria containing mutant grow a lower density but directly outcompete ancestor convert them into mutants via superinfection. Reduced therefore spreads throughout population, driven by weaponized Pf. Yet high intracellular replication facilitates another evolutionary conflict: "cheater miniphages" lacking capsid genes invade populations full-length within cells. Although both miniphages are most immune superinfection limiting receptor, hybrid vigor is extremely unstable, as classic Tragedy Commons scenario ensues results complete prophage loss. The entire cycle - hyperactivation miniphage invasion loss occur 24h, showcasing rapid coevolution phages. This study demonstrates , potentially many other species prophages, risk being exploited these runaway process reduces virus.

Language: Английский

Citations

0