Retracted. A dedicated translation factor controls the synthesis of the global regulator Fis

Abstract

Retraction to: The EMBO Journal (2004) 23, 3375–3385. doi:10.1038/sj.emboj.7600343
In the above report, we presented data indicating that BipA, a protein that shares sequence identity with translational elongation factors, is required for the expression of the transcriptional modulator Fis. As part of our ongoing studies into BipA, we discovered that we were unable to reproduce data presented in Figures 4 and 6C of the paper, which were generated by JGP when he was in CDOC's laboratory. Specifically, we have been unable to reproduce immunoblots indicating that BipA is required for the efficient expression of Fis protein and, using a reconstructed version of the plasmid pJGP1, find that there is no significant difference in the level of Fis translation in the presence or absence of BipA. While we are confident that the experiments concerning the interactions of BipA with 70S ribosomes are valid, we conclude that the results shown in Figures 4 and 6C are unsound and therefore wish to retract the paper.

Original Abstract:
BipA is a highly conserved protein with global regulatoryproperties in Escherichia coli. We show here that it functionsas a translation factor that is required specifically forthe expression of the transcriptional modulator Fis. BipAbinds to ribosomes at a site that coincides with that ofelongation factor G and has a GTPase activity that issensitive to high GDP:GTP ratios and stimulated by 70Sribosomes programmed with mRNA and aminoacylatedtRNAs. The growth rate-dependent induction of BipAallows the efficient expression of Fis, thereby modulatinga range of downstream processes, including DNA metabolismand type III secretion. We propose a model in whichBipA destabilizes unusually strong interactions betweenthe 50 untranslated region of fis mRNA and the ribosome.Since BipA spans phylogenetic domains, transcript-selectivetranslational control for the ‘fast-track’ expression ofspecific mRNAs may have wider significance.

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ORCID for Paul Skipp: orcid.org/0000-0002-2995-2959

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