MqsR Toxin may be a Potential Anti-biofilm and Anti-persistence Target in Burkholderia cenocenocepacia.

Burkholderia cenocepacia biofilm and persister cells cause chronic, hard-to-treat infections. This study investigated the role of the MqsR/MqsA toxin-antitoxin (TA) system in these processes. B. cenocepacia persisters were induced with ciprofloxacin (10x MIC). Gene expression of TA systems was analyzed via qRT-PCR in biofilms and persisters. Following key target identification, in silico modeling, docking, and peptide design were performed. Ciprofloxacin induced a persister state. The MqsR toxin gene was significantly upregulated during biofilm formation (6.8-fold) and in persister cells (p < 0.05). Structural modeling defined the MqsR/MqsA interaction interface, enabling the computational prediction of a candidate inhibitory peptide (KLLKILDRHPDLLAEV) that was predicted to dock effectively with the toxin in silico. The significant upregulation of MqsR in B. cenocepacia biofilms and persisters suggests a correlation between this toxin and the persistence phenotype. In silico modeling predicted a potential inhibitory peptide that could disrupt the MqsR/MqsA interaction; however, these computational findings require experimental validation.