Evidence for Rho-dependent control of a virulence switch in .

is a significant cause of infections in the healthcare setting. More recently, has been a leading cause of secondary bacterial pneumonia in patients infected with SARS-CoV-2 and the overall frequency of infection increased 78% during the COVID-19 pandemic. can exist in virulent or avirulent subpopulations and this interconversion is mediated by the expression of a family of TetR-type transcriptional regulators.

Stochastic activation of a family of TetR type transcriptional regulators controls phenotypic heterogeneity in .

Phenotypic heterogeneity is an important mechanism for regulating bacterial virulence, where a single regulatory switch is typically activated to generate virulent and avirulent subpopulations. The opportunistic pathogen can transition at high frequency between virulent opaque (VIR-O) and avirulent translucent subpopulations, distinguished by cells that form opaque or translucent colonies. We demonstrate that expression of 11 TetR-type transcriptional regulators (TTTRs) can drive cells from the VIR-O opaque subpopulation to cells that form translucent colonies.

A LysR-Type Transcriptional Regulator Controls Multiple Phenotypes in .

is a multidrug-resistant, Gram-negative nosocomial pathogen that exhibits phenotypic heterogeneity resulting in virulent opaque (VIR-O) and avirulent translucent (AV-T) colony variants. Each variant has a distinct gene expression profile resulting in multiple phenotypic differences. Cells interconvert between the VIR-O and AV-T variants at high frequency under laboratory conditions, suggesting that the genetic mechanism underlying the phenotypic switch could be manipulated to attenuate virulence.

Characterization of RelA in Acinetobacter baumannii.

In response to nutrient depletion, the RelA and SpoT proteins generate the signaling molecule (p)ppGpp, which then controls a number of downstream effectors to modulate cell physiology. In strain AB5075, a ortholog () was identified by a transposon insertion that conferred an unusual colony phenotype. An in-frame deletion in (Δ) failed to produce detectable levels of ppGpp when amino acid starvation was induced with serine hydroxamate.

Interaction between Streptococcus pneumoniae and Staphylococcus aureus Generates OH Radicals That Rapidly Kill Staphylococcus aureus Strains.

rapidly kills by producing membrane-permeable hydrogen peroxide (HO). The mechanism by which -produced HO mediates killing was investigated. An model that mimicked - contact during colonization of the nasopharynx demonstrated that killing required outcompeting densities of Compared to the wild-type strain, isogenic Δ and Δ, both deficient in production of HO, required increased density to kill While residual HO activity produced by single mutants was sufficient to eradicate , an Δ Δ double mutant was unable to kill A collection of 20 diverse methicillin-resistant (MRSA) and methicillin-susceptible (MSSA) strains showed linear sensitivity ( = 0.

Dauer life stage of Caenorhabditis elegans induces elevated levels of defense against the parasite Serratia marcescens.

Host-parasite research often focuses on a single host life stage, yet different life stages may exhibit different defenses. The nematode Caenorhabditis elegans has an alternate dispersal life stage, dauer. Despite dauer's importance in nature, we know little of how it responds to parasites.