THE RIFAMPICIN-INDUCIBLE GENES SRNB FROM F AND PND FROM R483 ARE REGULATED BY ANTISENSE RNAS AND MEDIATE PLASMID MAINTENANCE BY KILLING OF PLASMID-FREE SEGREGANTS

AK NIELSEN; P THORSTED; T THISTED; EGH WAGNER; Kenn Gerdes

doi:10.1111/j.1365-2958.1991.tb00818.x

THE RIFAMPICIN-INDUCIBLE GENES SRNB FROM F AND PND FROM R483 ARE REGULATED BY ANTISENSE RNAS AND MEDIATE PLASMID MAINTENANCE BY KILLING OF PLASMID-FREE SEGREGANTS

AK NIELSEN, P THORSTED, T THISTED, EGH WAGNER, Kenn Gerdes

42 Citationer (Scopus)

Abstract

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.

Originalsprog	Engelsk
Tidsskrift	Molecular Microbiology
Vol/bind	5
Udgave nummer	8
Sider (fra-til)	1961-1973
Antal sider	13
ISSN	0950-382X
DOI	https://doi.org/10.1111/j.1365-2958.1991.tb00818.x
Status	Udgivet - 1991
Udgivet eksternt	Ja

Adgang til dokumentet

10.1111/j.1365-2958.1991.tb00818.x

Citationsformater

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title = "THE RIFAMPICIN-INDUCIBLE GENES SRNB FROM F AND PND FROM R483 ARE REGULATED BY ANTISENSE RNAS AND MEDIATE PLASMID MAINTENANCE BY KILLING OF PLASMID-FREE SEGREGANTS",

abstract = "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.",

author = "AK NIELSEN and P THORSTED and T THISTED and EGH WAGNER and Kenn Gerdes",

year = "1991",

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T1 - THE RIFAMPICIN-INDUCIBLE GENES SRNB FROM F AND PND FROM R483 ARE REGULATED BY ANTISENSE RNAS AND MEDIATE PLASMID MAINTENANCE BY KILLING OF PLASMID-FREE SEGREGANTS

AU - NIELSEN, AK

AU - THORSTED, P

AU - THISTED, T

AU - WAGNER, EGH

AU - Gerdes, Kenn

PY - 1991

Y1 - 1991

N2 - 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.

AB - 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.

U2 - 10.1111/j.1365-2958.1991.tb00818.x

DO - 10.1111/j.1365-2958.1991.tb00818.x

M3 - Journal article

SN - 0950-382X

VL - 5

SP - 1961

EP - 1973

JO - Molecular Microbiology

JF - Molecular Microbiology

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