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Nucleic Acids Research, 2001, Vol. 29, No. 2 536-544
© 2001 Oxford University Press

Cnr interferes with dimerization of the replication protein {alpha} in phage-plasmid P4

Arianna Tocchetti, Stefania Serina, Ilaria Oliva, Gianni Dehò and Daniela Ghisotti*

Dipartimento di Genetica e di Biologia dei Microrganismi, Università di Milano, Via Celoria 26, 20133 Milano, Italy

DNA replication of phage-plasmid P4 in its host Escherichia coli depends on its replication protein {alpha}. In the plasmid state, P4 copy number is controlled by the regulator protein Cnr (copy number regulation). Mutations in {alpha} ({alpha}cr) that prevent regulation by Cnr cause P4 over-replication and cell death. Using the two-hybrid system in Saccharomyces cerevisiae and a system based on {lambda} immunity in E.coli for in vivo detection of protein–protein interactions, we found that: (i) {alpha} protein interacts with Cnr, whereas {alpha}cr proteins do not; (ii) both {alpha}–{alpha} and {alpha}cr–{alpha}cr interactions occur and the interaction domain is located within the C-terminal of {alpha}; (iii) Cnr–Cnr interaction also occurs. Using an in vivo competition assay, we found that Cnr interferes with both {alpha}–{alpha} and {alpha}cr–{alpha}cr dimerization. Our data suggest that Cnr and {alpha} interact in at least two ways, which may have different functional roles in P4 replication control.

* To whom correspondence should be addressed. Tel: +39 02 26605217; Fax: +39 02 2664551; Email: daniela.ghisotti{at}unimi.it Present addresses:Arianna Tocchetti, Department of Medical Biochemistry, University of Göteborg, Medicinaregatan 9A, Box 440, 40530 Göteborg, SwedenStefania Serina, Biosearch Italia, Via R. Lepetit 34, 21040 Gerenzano (VA), Italy


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