A novel quorum sensing regulator LuxT contributes to the virulence of .

is a waterborne bacterium that primarily infects the human intestine and causes cholera fatality. Quorum sensing (QS) negatively regulates the expression of virulence gene. However, the primary associated mechanisms remain undetermined. This investigation identified a new QS regulator from the TetR family, LuxT, which increases virulence by directly inhibiting expression. HapR is a master QS regulator that suppresses virulence cascade expression. The expression of increased 4.8-fold in the small intestine of infant mice than in Luria-Bertani broth. Δ mutant strain revealed a substantial defect in the colonizing ability of the small intestines. At low cell densities, the expression level of was upregulated by deletion, suggesting that LuxT can suppress transcription. The electrophoretic mobility shift analysis revealed that LuxT directly binds to the promoter region. Furthermore, expression was upregulated by the two-component system ArcB/ArcA, which responses to changes in oxygen levels in response to the host's small intestine's anaerobic signals. In conclusion, this research reveals a novel cell density-mediated virulence regulation pathway and contributes to understanding the complex association between virulence and QS signals. This evidence furnishes new insights for future studies on pathogenic mechanisms.