PtrB of Pseudomonas aeruginosa Suppresses the Type III Secretion System under the Stress of DNA Damage

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Abstract
In a search for regulatory genes of the type III secretion system (TTSS) in Pseudomonas aeruginosa , transposon (Tn 5 ) insertional mutants of the prtR gene were found defective in the TTSS. PrtR is an inhibitor of prtN , which encodes a transcriptional activator for pyocin synthesis genes. In P. aeruginosa , pyocin synthesis is activated when PrtR is degraded during the SOS response. Treatment of a wild-type P. aeruginosa strain with mitomycin C, a DNA-damaging agent, resulted in the inhibition of TTSS activation. A prtR / prtN double mutant had the same TTSS defect as the prtR mutant, and complementation by a prtR gene but not by a prtN gene restored the TTSS function. Also, overexpression of the prtN gene in wild-type PAK had no effect on the TTSS; thus, PrtN is not involved in the repression of the TTSS. To identify the PrtR-regulated TTSS repressor, another round of Tn mutagenesis was carried out in the background of a prtR / prtN double mutant. Insertion in a small gene, designated ptrB , restored the normal TTSS activity. Expression of ptrB is specifically repressed by PrtR, and mitomycin C-mediated suppression of the TTSS is also abolished in a ptrB mutant strain. Therefore, PtrB is a new TTSS repressor that coordinates TTSS repression and pyocin synthesis under the stress of DNA damage.
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