Virulence regulation in the fish pathogen Pseudomonas plecoglossicida: an integrated overview
TL;DR
The core functions of these virulence factors of Pseudomonas plecoglossicida are summarized and the molecular mechanisms by which this pathogen senses environmental signals and modulates virulence expression are dissected to provide a theoretical basis for the development of novel antivirulence strategies and therapeutic interventions.
Abstract
The genomes of pathogenic bacteria typically encode a diverse array of virulence factors, which constitute the fundamental basis for resisting host immunity and establishing infection. Given the high energetic cost of virulence gene expression, pathogens must precisely orchestrate the activation and silencing of these genes in accordance with the infection process, thereby flexibly executing diverse biological functions within the constraints of their energy budget. To sustain efficient infection, pathogens have evolved multiple mechanisms governing gene expression, enabling them to maintain competitive advantages over both their hosts and microbial competitors across diverse niches. Pseudomonas plecoglossicida is an important Gram-negative pathogen in aquaculture that combines strong environmental adaptability with host invasiveness. It frequently causes explosive epidemics such as visceral white spot disease, inflicting substantial economic losses, and represents one of the principal pathogens threatening the sustainability of aquaculture. An in-depth dissection of its complex virulence mechanisms and hierarchical regulatory networks will provide critical molecular insights into the dynamic interplay between P. plecoglossicida and its hosts. Accordingly, this review focuses on the key virulence factors of P. plecoglossicida, including secretion systems (the type III secretion system and its effector PP_ExoU, and the fish-pathogen-specific type VI secretion system T6SS-1), extracellular products, the flagellar system, metal nutrient acquisition systems, and outer membrane barriers, together with their hierarchical regulatory networks comprising sigma factors, two-component systems, quorum sensing, the second messenger cyclic di-GMP, and small RNAs. We summarize the core functions of these virulence factors and dissect the molecular mechanisms by which this pathogen senses environmental signals and modulates virulence expression, aiming to provide a theoretical basis for the development of novel antivirulence strategies and therapeutic interventions.