Information de reference pour ce titreAccession Number: | 00005797-200207020-00017.
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Author: | Pedersen, Kim; Christensen, Susanne K.; Gerdes, Kenn 1
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Institution: | Department of Biochemistry and Molecular Biology, University of Southern Denmark, DK-5230 Odense M, Denmark.
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Title: | |
Source: | Molecular Microbiology. 45(2):501-510, July 2002.
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Abstract: | Summary: 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.
(C) 2002 Blackwell Science Ltd.
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Language: | English.
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Document Type: | Research Articles.
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Journal Subset: | Life Sciences.
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ISSN: | 0950-382X
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NLM Journal Code: | mom, 8712028
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