The small RNA istR inhibits synthesis of an SOS-induced toxic peptide

Jörg Vogel*, Liron Argaman, E. Gerhart H. Wagner, Shoshy Altuvia

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

221 Scopus citations

Abstract

More than 60 small RNAs (sRNA) have been identified in E. coli [1-7]. The functions of the majority of these sRNAs are still unclear. For the few sRNAs characterized, expression and functional studies indicate that they act under stress conditions [8-14]. Here, we describe a novel E. coli chromosome locus that is part of the SOS response to DNA damage. This locus encodes two sRNAs, IstR-1 and IstR-2, and a toxic peptide, TisB, encoded by tisAB mRNA. Transcription of tisAB and istR-2 is SOS regulated, whereas IstR-1 is present throughout growth. IstR-1 inhibits toxicity by base-pairing to a short region in the tisAB mRNA. This antisense interaction entails RNase III-dependent cleavage, thereby inactivating the mRNA for translation. In the absence of the SOS response, IstR-1 is present in high excess over its target. However, SOS induction leads to depletion of the IstR-1 pool, concomitant with accumulation of tisAB mRNA. Under such conditions, TisB exerts its toxic effect, slowing down growth. We propose that the inhibitory sRNA prevents inadvertent TisB synthesis during normal growth and, possibly, also limits SOS-induced toxicity. Our study adds the SOS regulon to the growing list of global regulatory circuits controlled by sRNA genes.

Original languageAmerican English
Pages (from-to)2271-2276
Number of pages6
JournalCurrent Biology
Volume14
Issue number24
DOIs
StatePublished - 29 Dec 2004

Bibliographical note

Funding Information:
We thank Roger Woodgate and Zvi Livneh for strains, Gisela Storz and Kenn Gerdes for comments on the manuscript, and Santanu Dasgupta for constructing the rnc14 derivatives of the strains used in this study. We acknowledge support from the Israel Science Foundation founded by the Israel Academy of Sciences and Humanities, grant number 663/02 (S.A.), the United States-Israel Binational Science Foundation, grant number 2001032 (S.A.), Intramural Research Funds from the Hebrew University (S.A.), the Swedish Research Council (G.W.), the Wallenberg Consortium North (G.W.), the Swedish Foundation for Strategic Research (G.W.), the Human Frontier Science Program (G.W. and S.A.), and the European Molecular Biology Organisation for a long-term fellowship (J.V.).

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