Chemotactic-signal transducers respond to changes in the concentration of attractants and repellents in the environment, transduce a signal from the outside to the inside of the cell, and facilitate sensory adaptation through the variation of the level of methylation. Major receptor that responds to all naturally occurring L-amino acids, except L-Gln and L-Asp. Also involved in repellent responses to trichloroethylene (TCE), chloroform and methylthiocyanate (PubMed:16233808, PubMed:23650915, PubMed:8522505, PubMed:9353923). Also mediates chemotaxis to histamine, but does not bind histamine (PubMed:30425146). In addition, binds the quorum-sensing signal autoinducer 2 (AI-2), thus inducing chemotaxis toward AI-2 and biofilm formation (PubMed:33097715). Monomer in the absence and presence of ligands. The ligand binding region binds directly to 17 L-amino acids. Mutant is defective in taxis toward 17 amino acids, including Gly, L-Ser, L-Thr and L-Val. Mutant shows also decreased chemotactic responses to TCE, chloroform and methylthiocyanate (PubMed:16233808, PubMed:8522505, PubMed:9353923). Deletion of pctA, pctB and pctC abolishes chemotaxis to 5 mM histamine, but significant chemotaxis is observed at a concentration range between 500 nM and 500 uM (PubMed:30425146). The pctABC-tlpQ deletion mutant is devoid of histamine chemotaxis over the entire concentration range (50 nM to 50 mM) (PubMed:30425146). Deletion of the gene significantly reduces chemotaxis to AI-2 (PubMed:33097715). The deletion mutant does not show significant reduction in swarming or immobilization near epithelial wounds, but the pctABC triple deletion mutant shows a significant reduction in chemotaxis and immobilization along wounds of human cystic fibrosis airway epithelial cells (PubMed:27031335). PctA has a broad ligand range and responds to most of the proteinogenic amino acids, whereas PctB and PctC have a much narrower range and show strong ligand preference for L-glutamine and gamma-aminobutyrate, respectively. These receptors are paralogs: pctA gene duplication in the common ancestor of the genus Pseudomonas led to pctC, whereas pctB originated through another, independent pctA duplication. Belongs to the methyl-accepting chemotaxis (MCP) protein family.