The effect of pmpR on the type Ⅲ secretion system in Pseudomonas aeruginosa

The type III secretion system(T3SS) plays important roles in Pseudomonas aeruginosa pathogenicity.Previously,we reported that the uncharacterized protein PmpR could regulate pqsR,an important regulator in the quorum-sensing system,by directly binding to its promoter region.As the T3SS is controlled by the quorum-sensing system,here,we investigated the relationship between PmpR and the T3SS.Our data showed that expression of the T3SS genes exoS,exoY,exoT,and exsD was dramatically increased in a pmpR-deletion mutant compared with that in the wild-type P.aeruginosa strain PAO1.Data from DNA mobility assays indicated that PmpR affects the T3SS indirectly.It is unlikely that PmpR controls the T3SS via the Pseudomonas quinolone signal(PQS) because the PQS negatively regulates the T3SS,while pmpR negatively regulates the PQS.The effect of PmpR on the T3SS seems to be independent of the PQS;further investigation is required to uncover the underlying regulatory pathways.

The type Ⅲ secretion system （T3SS） plays important roles in Pseudomonas aeruginosa pathogenicity. Previously, we reported that the uncharacterized protein PmpR could regulate pqsR, an important regulator in the quorum-sensing system, by directly binding to its promoter region. As the T3SS is controlled by the quorum-sensing system, here, we investigated the relationship between PmpR and the T3SS. Our data showed that expression of the T3SS genes exoS, exoY, exoT, and exsD was dramatically increased in a pmpR-deletion mutant compared with that in the wild-type P. aeruginosa strain PAO1. Data from DNA mobility assays indicated that PmpR affects the T3SS indirectly. It is unlikely that PmpR controls the T3SS via the Pseudomonas quino- lone signal （PQS） because the PQS negatively regulates the T3SS, while pmpR negatively regulates the PQS. The effect of PmpR on the T3SS seems to be independent of the PQS; further investigation is required to uncover the underlying regulatory pathways.