T. K. Wood

This study shows bacteria can survive phage infection through mutation or by forming persisters, which survive without mutation and retain wild-type phage sensitivity.

This paper develops a high-throughput assay to identify small molecules active against persister cells by optimizing conditions to generate high concentrations of tolerant S. aureus cells.

The paper shows that cryptic prophages in E. coli regulate phosphate uptake to control persister cell resuscitation, preventing premature resuscitation in nutrient-poor conditions.

This study shows that indole inhibits Pseudomonas aeruginosa persister cell resuscitation, suggesting a mechanism by which commensal bacteria like E. coli outcompete pathogens.

The paper proposes a model linking ppGpp to bacterial persistence through ribosome inactivation by RMF and Hpf, showing ppGpp does not affect single-cell resuscitation.

The paper identifies that persister cells wake by sensing nutrients via chemotaxis, reducing cAMP, and reviving ribosomes, using E. coli as a model.

This study shows that Pseudomonas aeruginosa supernatants, containing rhamnolipids, effectively disperse biofilms of sulfate-reducing bacteria and other microbes.

The paper uses microscopy to study persister cells in E. coli and finds that their resuscitation rate correlates with ribosome content.

This study shows that viable but non-culturable (VBNC) cells and persisters are the same dormant phenotype, as both are metabolically inactive and only persisters can resuscitate.