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Journal of Bacteriology, September 2005, p. 5977-5983, Vol. 187, No. 17
0021-9193/05/$08.00+0     doi:10.1128/JB.187.17.5977-5983.2005

Species and Incompatibility Determination within the P1par Family of Plasmid Partition Elements

Alena Dabrazhynetskaya, Kirill Sergueev, and Stuart Austin*

Gene Regulation and Chromosome Biology Laboratory, National Cancer Institute, CCR, NCI-Frederick, Frederick, Maryland 21702-1201

Received 25 March 2005/ Accepted 10 June 2005

The P1par family of active plasmid partition systems consists of at least six members, broadly distributed in a variety of plasmid types and bacterial genera. Each encodes two Par proteins and contains a cis-acting parS site. Individual par systems can show distinct species specificities; the proteins from one type cannot function with the parS site of another. P1par-versus-P7par specificity resides within two hexamer BoxB repeats encoded by parS that contact the ParB protein near the carboxy terminus. Here, we examine the species specificity differences between Yersinia pestis pMT1parS and Escherichia coli P1 and P7parS. pMT1parS site specificity could be altered to that of either P1 or P7 by point mutation changes in the BoxB repeats. Just one base change in a single BoxB repeat sometimes sufficed. The BoxB sequence appears to be able to adopt a number of forms that define exclusive interactions with different ParB species. The looped parS structure may facilitate this repertoire of interaction specificities. Different P1par family members have different partition-mediated incompatibility specificities. This property defines whether two related plasmids can coexist in the same cell and is important in promoting the evolution of new plasmid species. BoxB sequence changes that switch species specificity between P1, P7, and pMT1 species switched partition-mediated plasmid incompatibility in concert. Thus, there is a direct mechanistic link between species specificity and partition-mediated incompatibility, and the BoxB-ParB interaction can be regarded as a special mechanism for facilitating plasmid evolution.


* Corresponding author. Mailing address: Gene Regulation & Chromosome Biology Laboratory, National Cancer Institute, CCR, NCI-Frederick, Frederick, MD 21702-1201. Phone: (301) 846-1266. Fax: (301) 846-6988. E-mail: austin{at}ncifcrf.gov.


Journal of Bacteriology, September 2005, p. 5977-5983, Vol. 187, No. 17
0021-9193/05/$08.00+0     doi:10.1128/JB.187.17.5977-5983.2005




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