Abstract:
:parD and chpA are homologous conditional killer systems of plasmid and chromosomal origin, respectively, encoding a killer protein (Kid and ChpAK) and an antidote (Kis and ChpAI). Here it is shown that these systems can functionally interact. A multicopy chpA recombinant partially complements two mutations in the antidote of the parD system. These mutations affect either autoregulation or neutralization of the killer component. Following in vitro mutagenesis with hydroxylamine, chpA mutants that improve this complementation were isolated. Sequence analysis shows that these mutants are clustered in the 5' end of the chpAI gene and structure predictions suggest that they affect a putative loop in the secondary structure of the ChpAI antidote. It is proposed that this region is part of a protein-protein interface required for the functional interaction between the antidote and the killer components in the two homologous systems.
journal_name
FEMS Microbiol Lettjournal_title
FEMS microbiology lettersauthors
Santos-Sierra S,Giraldo R,Díaz-Orejas Rdoi
10.1111/j.1574-6968.1997.tb10408.xsubject
Has Abstractpub_date
1997-07-01 00:00:00pages
51-6issue
1eissn
0378-1097issn
1574-6968pii
S0378-1097(97)00177-8journal_volume
152pub_type
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