# Genomic and Metabolic Characteristics of the Pathogenicity in Pseudomonas aeruginosa
## 4 Metabolic Pathways Associated with Pathogenicity
### Virulence Factors
#### 4.1.2 Motility  
In bacteria, motility plays a fundamental role in the colonization of abiotic surfaces (e.g., medical devices) and biotic surfaces (e.g., damaged tissues), as well as in the spreading of bacteria across the surface [98], thereby contributing to virulence. Motility contributes to the formation of biofilm and, consequently, the formation of problematic bacterial communities, with increased resistance to antimicrobial agents [99]. In _P. aeruginosa_, cell surface organelles, flagella, and pili are used for motility. The surface-associated, twitching motility, is dependent on the extension and retraction of type IV pili. The flagellum allows this bacterium to swim in liquid media and swarm across a solid surface (Figure 3) [100; 101].  
_P. aeruginosa_ has a single polar flagellum, composed of a flagellin protein named FliC [3]. The flagellum consists of a basal body and a motor situated within the cell membrane, and of a rod which extends through the peptidoglycan and outer layers of the cell, to which the hook and filament are attached (Figure 4). Swimming and swarming actions are driven by rotation of the flagellum, which allows _P. aeruginosa_ to move. Forward propulsion results from an anti-clockwise rotation of the flagellum, while tumbling motion results from its clockwise revolution. Changes in the direction of movement result from chemotaxis and are triggered by chemical signals [100; 102].  
Twitching motility involves the movement of cell surface appendages called pili. In _P. aeruginosa_, type IV pili (T4P) are the specific pili. These pili are synthesized within the cell and this process involves a series of proteins (PiLA, PiLC, PiLB, PiIQ) that intervene in the rapid assembly and disassembly, leading to a twitching movement [103]. This movement results in small clusters of cells that come together to form a networked cell structure, with the vanguard actively involved in migration, fixation, and biofilm formation [100; 104]. The nucleotide signaling molecule cyclic-di-GMP controls sessile motility switch. The cyclic-di-GMP regulates a transition from the mobile and planktonic state to sessile, favoring biofilm development, by inhibiting the flagella and pili that allow for this type of movement. When levels of this nucleotide signaling molecule are low, a motile lifestyle is favored [103]. [PERSON] and his collaborators show that some of the two-component systems biofilm regulators regulate flagellum-dependent swimming motility and type IV pilus-dependent contraction motility. For example, when comparing the two-component system mutants with their isogenic parent _P. aeruginosa_ PA14 (using controls PA14_nll_ as positive control and PA14_pilW_ and negative control), it was demonstrated that parent PA14 and PA14_nll_ were capable of twitching but not the PA14_pilW_ mutant [105].Thus, motility is a virulence factor that is essential for several functions, such as surface detection and translocation, lifestyle change, and biofilm formation. Motility and adherence seem to play important roles in triggering host immune responses, biofilm formation, and the development of chronic infection [3].  
Figure 3: The three types of bacterial motility which _Pseudomonas aeruginosa_. The cell’s direction of movement is represented by dark blue arrows, and the motors that drive the movement are represented by red arrows.