Rapid induction and reversal of a bacteriostatic condition by controlled expression of toxins and antitoxins

K Pedersen; SK Christensen; K Gerdes

doi:10.1046/j.1365-2958.2002.03027.x

Rapid induction and reversal of a bacteriostatic condition by controlled expression of toxins and antitoxins

K Pedersen, SK Christensen, K Gerdes

297 Citationer (Scopus)

Abstract

RelE and ChpAK (MazF) toxins of Escherichia coli have previously been described as proteins that mediate efficient cell killing. We show here that induction of relE or chpAK transcription does not confer cell killing but, instead, induces a static condition in which the cells are still viable but unable to proliferate. Later induction of transcription of the antitoxin genes relB or chpAI fully reversed the static condition induced by RelE and ChpAK respectively. We also provide a mechanistic explanation for these findings. Thus, induction of relE transcription severely inhibited translation, whereas induction of chpAK transcription inhibited both translation and replication. Hence, most likely, lack of colony formation is due to inhibition of translation in the case of relE and inhibition of translation and/or replication in the case of chpAK . Consistent with this proposal, later induction of transcription of the cognate antitoxin genes simultaneously reversed cell stasis and the inhibitory effects of RelE and ChpAK on macromolecular syntheses. These results preclude that RelE and ChpAK mediate cell killing during the conditions used here. In vivo and in vitro analyses of a mutant RelE protein supported that inhibition of colony formation was due to inhibition of translation.

Originalsprog	Engelsk
Tidsskrift	Molecular Microbiology
Vol/bind	45
Udgave nummer	2
Sider (fra-til)	501-510
Antal sider	10
ISSN	0950-382X
DOI	https://doi.org/10.1046/j.1365-2958.2002.03027.x
Status	Udgivet - 2002
Udgivet eksternt	Ja

Adgang til dokumentet

10.1046/j.1365-2958.2002.03027.x

Citationsformater

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title = "Rapid induction and reversal of a bacteriostatic condition by controlled expression of toxins and antitoxins",

abstract = "RelE and ChpAK (MazF) toxins of Escherichia coli have previously been described as proteins that mediate efficient cell killing. We show here that induction of relE or chpAK transcription does not confer cell killing but, instead, induces a static condition in which the cells are still viable but unable to proliferate. Later induction of transcription of the antitoxin genes relB or chpAI fully reversed the static condition induced by RelE and ChpAK respectively. We also provide a mechanistic explanation for these findings. Thus, induction of relE transcription severely inhibited translation, whereas induction of chpAK transcription inhibited both translation and replication. Hence, most likely, lack of colony formation is due to inhibition of translation in the case of relE and inhibition of translation and/or replication in the case of chpAK . Consistent with this proposal, later induction of transcription of the cognate antitoxin genes simultaneously reversed cell stasis and the inhibitory effects of RelE and ChpAK on macromolecular syntheses. These results preclude that RelE and ChpAK mediate cell killing during the conditions used here. In vivo and in vitro analyses of a mutant RelE protein supported that inhibition of colony formation was due to inhibition of translation.",

author = "K Pedersen and SK Christensen and K Gerdes",

year = "2002",

doi = "10.1046/j.1365-2958.2002.03027.x",

language = "English",

volume = "45",

pages = "501--510",

journal = "Molecular Microbiology",

issn = "0950-382X",

publisher = "Wiley-Blackwell",

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TY - JOUR

T1 - Rapid induction and reversal of a bacteriostatic condition by controlled expression of toxins and antitoxins

AU - Pedersen, K

AU - Christensen, SK

AU - Gerdes, K

PY - 2002

Y1 - 2002

N2 - RelE and ChpAK (MazF) toxins of Escherichia coli have previously been described as proteins that mediate efficient cell killing. We show here that induction of relE or chpAK transcription does not confer cell killing but, instead, induces a static condition in which the cells are still viable but unable to proliferate. Later induction of transcription of the antitoxin genes relB or chpAI fully reversed the static condition induced by RelE and ChpAK respectively. We also provide a mechanistic explanation for these findings. Thus, induction of relE transcription severely inhibited translation, whereas induction of chpAK transcription inhibited both translation and replication. Hence, most likely, lack of colony formation is due to inhibition of translation in the case of relE and inhibition of translation and/or replication in the case of chpAK . Consistent with this proposal, later induction of transcription of the cognate antitoxin genes simultaneously reversed cell stasis and the inhibitory effects of RelE and ChpAK on macromolecular syntheses. These results preclude that RelE and ChpAK mediate cell killing during the conditions used here. In vivo and in vitro analyses of a mutant RelE protein supported that inhibition of colony formation was due to inhibition of translation.

AB - RelE and ChpAK (MazF) toxins of Escherichia coli have previously been described as proteins that mediate efficient cell killing. We show here that induction of relE or chpAK transcription does not confer cell killing but, instead, induces a static condition in which the cells are still viable but unable to proliferate. Later induction of transcription of the antitoxin genes relB or chpAI fully reversed the static condition induced by RelE and ChpAK respectively. We also provide a mechanistic explanation for these findings. Thus, induction of relE transcription severely inhibited translation, whereas induction of chpAK transcription inhibited both translation and replication. Hence, most likely, lack of colony formation is due to inhibition of translation in the case of relE and inhibition of translation and/or replication in the case of chpAK . Consistent with this proposal, later induction of transcription of the cognate antitoxin genes simultaneously reversed cell stasis and the inhibitory effects of RelE and ChpAK on macromolecular syntheses. These results preclude that RelE and ChpAK mediate cell killing during the conditions used here. In vivo and in vitro analyses of a mutant RelE protein supported that inhibition of colony formation was due to inhibition of translation.

U2 - 10.1046/j.1365-2958.2002.03027.x

DO - 10.1046/j.1365-2958.2002.03027.x

M3 - Journal article

SN - 0950-382X

VL - 45

SP - 501

EP - 510

JO - Molecular Microbiology

JF - Molecular Microbiology

IS - 2

ER -