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The rifampicin‐inducible genes srn6 from F and pnd from R483 are regulated by antisense RNAs and mediate plasmid maintenance by kiiling of plasmid‐free segregants
Author(s) -
Nielsen A. K.,
Thorsted P.,
Thisted T.,
Wagner E. G. H.,
Gerdes K.
Publication year - 1991
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.1991.tb00818.x
Subject(s) - plasmid , biology , antisense rna , rna , gene , sense (electronics) , microbiology and biotechnology , rnase p , genetics , chemistry
Summary The gene systems srnB of plasmid F and pnd of plasmid R483 were discovered because of their induction by rifampicin. Induction caused membrane damage, RNase I influx, degradation of stable RNA and, consequently, cell killing. We show here that the srnB and pnd systems mediate efficient stabilization of a mini‐R1 test‐plasmid. We also show that the killer genes srnB ′ and pndA are regulated by antisense RNAs, and that the srnC ‐ and pndB ‐encoded antisense RNAs, denoted SrnC‐ and PndB‐RNAs, are unstable molecules of approximately 60 nucleotides. The srnB and pndA mRNAs were found to be very stable. The differential decay rates of the inhibitory antisense RNAs and the killer‐gene‐encoding mRNAs explain the induction of these gene systems by rifampicin. Furthermore, the observed plasmid‐stabilization phenotype associated with the srnB and pnd systems is a consequence of this differential RNA decay: the newborn plasmid‐free cells inherit the stable mRNAs, which, after decay of the unstable antisense RNAs, are translated Into killer proteins, thus leading to selective killing of the plasmid‐free segregants. Thus our observations lead us to conclude that the F srnB and R483 pnd systems are phenotypically indistinguishable from the R1 hok/sok system, despite a 50% dissimilarity at the level of DNA sequence.