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Cnr interferes with dimerization of the replication protein alpha in phage-plasmid P4
Author(s) -
Arianna Tocchetti,
Stefania Serina,
Ilaria Oliva,
Gianni Dehò,
Daniela Ghisotti
Publication year - 2001
Publication title -
nucleic acids research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 9.008
H-Index - 537
eISSN - 1362-4954
pISSN - 0305-1048
DOI - 10.1093/nar/29.2.536
Subject(s) - biology , lambda phage , plasmid , alpha (finance) , dna replication , microbiology and biotechnology , saccharomyces cerevisiae , dna , escherichia coli , origin of replication , genetics , bacteriophage , gene , nursing , patient satisfaction , medicine , construct validity
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.

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