Article

  • The EMBO Journal (2006) 25, 512 - 521
  • doi:10.1038/sj.emboj.7600961

Published online: 26 January 2006

Recruitment of Tup1p and Cti6p regulates heme-deficient expression of Aft1p target genes

Robert J Crisp, Erika M Adkins, Emily Kimmel and Jerry Kaplan

  1. Department of Pathology, School of Medicine, University of Utah, Salt Lake City, UT, USA

Correspondence to:

Jerry Kaplan, Department of Pathology, School of Medicine, University of Utah, 50 North Medical Drive, 1900 East, Salt Lake City, UT 84132-2501, USA. Tel.: +1 801 581 7427; Fax: +1 801 581 6001; E-mail: jerry.kaplan@path.utah.edu

Received 18 October 2005; Accepted 20 December 2005


In the budding yeast Saccharomyces cerevisiae, transcription of genes encoding for the high-affinity iron (FET3, FTR1) and copper (CTR1) transporters does not occur in the absence of heme. We show that the Aft1p binding region of the FET3 promoter or the Mac1p binding region of the CTR1 promoter is necessary and sufficient to mediate heme-deficient repression. Transcription is repressed in the absence of heme, and a genetic screen identified Tup1p and Hda1p as being required for transcriptional repression. In contrast to FET3 and CTR1, Aft1p target genes ARN1 and FIT1 are transcribed in the absence of heme. A 14 bp sequence in the ARN1 promoter is necessary and sufficient to permit transcription in the absence of heme. Transcription in the absence of heme required the presence of Cti6p to overcome the effect of Tup1p, and Cti6p was recruited to the ARN1 promoter in the absence of heme. We hypothesize that transcription of the siderophore transporter ARN1 permits yeast to accumulate iron in the absence of oxygen and to deny iron to competing organisms.

  • Keywords:

    • Aft1p,
    • Cti6p,
    • heme,
    • iron,
    • Tup1p