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1. Competition between Solvent–Solvent and Solvent–Solute Interactions in the Microhydration of the Hexafluorophosphate Anion, PF 6 – (H 2 O) n=1,2

   https://doi.org/10.1021/acs.jpca.0c06466  

   Abdo, Yasmeen A. ; Tschumper, Gregory S. ( October 2020 , The Journal of Physical Chemistry A)

   null (Ed.)
2. Identification of Novel 2,4,5-Trisubstituted Pyrimidines as Potent Dual Inhibitors of Plasmodial Pf GSK3/ Pf PK6 with Activity against Blood Stage Parasites In Vitro

   https://doi.org/10.1021/acs.jmedchem.2c00996  

   Galal, Kareem A. ; Truong, Anna ; Kwarcinski, Frank ; de Silva, Chandi ; Avalani, Krisha ; Havener, Tammy M. ; Chirgwin, Michael E. ; Merten, Eric ; Ong, Han Wee ; Willis, Caleb ; et al ( September 2022 , Journal of Medicinal Chemistry)
3. A VSEPR-inspired force field for determining molecular properties of PF 5

   https://doi.org/10.1080/00268976.2018.1543907  

   McCaslin, Laura M. ; Stanton, John F. ( November 2018 , Molecular Physics)
4. Inhibition of PQS signaling by the Pf bacteriophage protein PfsE enhances viral replication in Pseudomonas aeruginosa

   https://doi.org/10.1111/mmi.15202  

   Schwartzkopf, Caleb M. ; Taylor, Véronique L. ; Groleau, Marie‐Christine ; Faith, Dominick R. ; Schmidt, Amelia K. ; Lamma, Tyrza L. ; Brooks, Diane M. ; Déziel, Eric ; Maxwell, Karen L. ; Secor, Patrick R. ( December 2023 , Molecular Microbiology)

   Quorum sensing, a bacterial signaling system that coordinates group behaviors as a function of cell density, plays an important role in regulating viral (phage) defense mechanisms in bacteria. The opportunistic pathogenPseudomonas aeruginosais a model system for the study of quorum sensing.P. aeruginosais also frequently infected by Pf prophages that integrate into the host chromosome. Upon induction, Pf phages suppress host quorum sensing systems; however, the physiological relevance and mechanism of suppression are unknown. Here, we identify the Pf phage protein PfsE as an inhibitor ofPseudomonasQuinolone Signal (PQS) quorum sensing. PfsE binds to the host protein PqsA, which is essential for the biosynthesis of the PQS signaling molecule. Inhibition of PqsA increases the replication efficiency of Pf virions when infecting a new host and when the Pf prophage switches from lysogenic replication to active virion replication. In addition to inhibiting PQS signaling, our prior work demonstrates that PfsE also binds to PilC and inhibits type IV pili extension, protectingP. aeruginosafrom infection by type IV pili‐dependent phages. Overall, this work suggests that the simultaneous inhibition of PQS signaling and type IV pili by PfsE may be a viral strategy to suppress host defenses to promote Pf replication while at the same time protecting the susceptible host from competing phages.

    

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5. Virulence as a Side Effect of Interspecies Interaction in Vibrio Coral Pathogens

   https://doi.org/10.1128/mBio.00201-20  

   Rubio-Portillo, Esther ; Martin-Cuadrado, Ana B. ; Caraballo-Rodríguez, Andrés M. ; Rohwer, Forest ; Dorrestein, Pieter C. ; Antón, Josefa ( August 2020 , mBio)

   Dubilier, Nicole (Ed.)

   ABSTRACT The increase in prevalence and severity of coral disease outbreaks produced by Vibrio pathogens, and related to global warming, has seriously impacted reef-building corals throughout the oceans. The coral Oculina patagonica has been used as a model system to study coral bleaching produced by Vibrio infection. Previous data demonstrated that when two coral pathogens ( Vibrio coralliilyticus and Vibrio mediterranei ) simultaneously infected the coral O. patagonica , their pathogenicity was greater than when each bacterium was infected separately. Here, to understand the mechanisms underlying this synergistic effect, transcriptomic analyses of monocultures and cocultures as well as experimental infection experiments were performed. Our results revealed that the interaction between the two vibrios under culture conditions overexpressed virulence factor genes (e.g., those encoding siderophores, the type VI secretion system, and toxins, among others). Moreover, under these conditions, vibrios were also more likely to form biofilms or become motile through induction of lateral flagella. All these changes that occur as a physiological response to the presence of a competing species could favor the colonization of the host when they are present in a mixed population. Additionally, during coral experimental infections, we showed that exposure of corals to molecules released during V. coralliilyticus and V. mediterranei coculture induced changes in the coral microbiome that favored damage to coral tissue and increased the production of lyso-platelet activating factor. Therefore, we propose that competition sensing, defined as the physiological response to detection of harm or to the presence of a competing Vibrio species, enhances the ability of Vibrio coral pathogens to invade their host and cause tissue necrosis. IMPORTANCE Vibrio coralliilyticus and Vibrio mediterranei are important coral pathogens capable of inducing serious coral damage, which increases severely when they infect the host simultaneously. This has consequences related to the dispersion of these pathogens among different locations that could enhance deleterious effects on coral reefs. However, the mechanisms underlying this synergistic interaction are unknown. The work described here provides a new perspective on the complex interactions among these two Vibrio coral pathogens, suggesting that coral infection could be a collateral effect of interspecific competition. Major implications of this work are that (i) Vibrio virulence mechanisms are activated in the absence of the host as a response to interspecific competition and (ii) release of molecules by Vibrio coral pathogens produces changes in the coral microbiome that favor the pathogenic potential of the entire Vibrio community. Thus, our results highlight that social cues and competition sensing are crucial determinants of development of coral diseases. 

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