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Eukaryotic Cell, November 2005, p. 1840-1850, Vol. 4, No. 11
1535-9778/05/$08.00+0     doi:10.1128/EC.4.11.1840-1850.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Activation of AP-1-Dependent Transcription by a Truncated Translation Initiation Factor{dagger}

Caroline C. L. Jenkins,1 Juan Mata,2 Richard F. Crane,3 Benjamin Thomas,1 Alexandre Akoulitchev,1 Jürg Bähler,2 and Chris J. Norbury1*

Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, United Kingdom,1 The Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, United Kingdom,2 Department of Cell Biology, Harvard Medical School, Boston, MA 021153

Received 5 July 2005/ Accepted 8 September 2005

Int6/eIF3e is a highly conserved subunit of eukaryotic translation initiation factor 3 (eIF3) that has also been reported to interact with subunits of the proteasome and the COP9 signalosome. Overexpression of full-length Int6 or a 13-kDa C-terminal fragment, Int6CT, in the fission yeast Schizosaccharomyces pombe causes multidrug resistance that requires the otherwise inessential AP-1 transcription factor Pap1. Here we show for the first time that Int6CT acts to increase the transcriptional activity of Pap1. Microarray hybridization data indicate that Int6CT overexpression resulted in the up-regulation of 67 genes; this expression profile closely matched that of cells overexpressing Pap1. Analysis of the upstream regulatory sequences of these genes showed that the majority contained AP-1 consensus binding sites. Partial defects in ubiquitin-dependent proteolysis have been suggested to confer Pap1-dependent multidrug resistance, but no such defect was seen on Int6CT overexpression. Indeed, none of the previously identified interactions of endogenous Int6 was required for the activation of Pap1 transcription described here. Moreover, Int6CT-induced activation of Pap1-responsive gene expression was independent of the ability of Pap1 to undergo a redox-regulated conformational change which mediates its relocalization to the nucleus and expression of oxidative stress response genes. Int6CT therefore activates Pap1-dependent transcription by a novel mechanism.

* Corresponding author. Mailing address: Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, United Kingdom. Phone: 44 1865 275540. Fax: 44 1865 275501. E-mail: chris.norbury{at}path.ox.ac.uk.

{dagger} Supplemental material for this article may be found at http://ec.asm.org/.

Eukaryotic Cell, November 2005, p. 1840-1850, Vol. 4, No. 11
1535-9778/05/$08.00+0     doi:10.1128/EC.4.11.1840-1850.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Chen, D., Wilkinson, C. R.M., Watt, S., Penkett, C. J., Toone, W. M., Jones, N., Bahler, J. (2008). Multiple Pathways Differentially Regulate Global Oxidative Stress Responses in Fission Yeast. Mol. Biol. Cell 19: 308-317 [Abstract] [Full Text]  


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