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Journal of Bacteriology, April 2007, p. 2599-2609, Vol. 189, No. 7
0021-9193/07/$08.00+0     doi:10.1128/JB.01680-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Regulatory Role of PopN and Its Interacting Partners in Type III Secretion of Pseudomonas aeruginosa{triangledown} ,{dagger}

Hongjing Yang,1,2 Zhiying Shan,1 Jaewha Kim,3 Weihui Wu,1 Wei Lian,1 Lin Zeng,1 Laijun Xing,2 and Shouguang Jin1*

Department of Molecular Genetics and Microbiology, P.O. Box 100266, University of Florida, Gainesville, Florida 32610-0266,1 Department of Microbiology, Institute of Life Sciences, Nankai University, Tianjin, Peoples Republic of China,2 Korea Research Institute of Bioscience and Biotechnology, Taejon 305-600, Republic of Korea3

Received 30 October 2006/ Accepted 8 January 2007

The type III secretion system (T3SS) of Pseudomonas aeruginosa plays a significant role in pathogenesis. We have previously identified type III secretion factor (TSF), which is required for effective secretion of the type III effector molecules, in addition to the low calcium signal. TSF includes many low-affinity high-capacity calcium binding proteins, such as serum albumin and casein. A search for the TSF binding targets on the bacterial outer membrane resulted in identification of PopN, a component of the T3SS that is readily detectable on the bacterial cell surface. PopN specifically interacts with Pcr1, and both popN and pcr1 mutants have a constitutive type III secretion phenotype, suggesting that the two proteins form a complex that functions as a T3SS repressor. Further analysis of the popN operon genes resulted in identification of protein-protein interactions between Pcr1 and Pcr4 and between Pcr4 and Pcr3, as well as between PopN and Pcr2 in the presence of PscB. Unlike popN and pcr1 mutants, pcr3 and pcr4 mutants are totally defective in type III secretion, while a pcr2 mutant exhibits reduced type III secretion. Interestingly, PopN, Pcr1, Pcr2, and Pcr4 are all secreted in a type III secretion machinery-dependent manner, while Pcr3 is not. These findings imply that these components have important regulatory roles in controlling type III secretion.

* Corresponding author. Mailing address: Department of Molecular Genetics and Microbiology, P.O. Box 100266, University of Florida, Gainesville, FL 32610-0266. Phone: (352) 392-8323. Fax: (352) 392-3133. E-mail: sjin{at}mgm.ufl.edu.

{triangledown} Published ahead of print on 19 January 2007.

{dagger} Supplemental material for this article may be found at http://jb.asm.org/.

Journal of Bacteriology, April 2007, p. 2599-2609, Vol. 189, No. 7
0021-9193/07/$08.00+0     doi:10.1128/JB.01680-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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