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J Biol Chem, Vol. 274, Issue 51, 36252-36260, December 17, 1999
From the Copper and iron serve essential functions as
catalytic co-factors in a wide variety of critical cellular enzymes.
Studies in yeast have demonstrated an absolute dependence upon copper acquisition for proper assembly and function of the iron transport machinery. We have cloned genes for a high affinity copper transporter (Ctr4) and copper-sensing transcription factor (Cuf1) from
Schizosaccharomyces pombe. Interestingly, the primary
structure of Ctr4 and a putative human high affinity copper transport
protein, hCtr1, suggests that they are derived from a fusion of the
functionally redundant but structurally distinct Ctr1 and Ctr3 copper
transporters from Saccharomyces cerevisiae. Furthermore,
although Cuf1 activates ctr4+ gene expression
under copper starvation conditions, under these same conditions Cuf1
directly represses expression of genes encoding components of the iron
transport machinery. These studies have identified an evolutionary step
in which copper transport modules have been fused, and describe a
mechanism by which a copper-sensing factor directly represses
expression of the iron uptake genes under conditions in which the
essential copper co-factor is scarce.
The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) AF175404 and AF175405.
A Copper-sensing Transcription Factor Regulates Iron Uptake Genes
in Schizosaccharomyces pombe*
§,¶,
**, and
Department of Biological Chemistry,
University of Michigan Medical School, Ann Arbor, Michigan 48109-0606 and Centro de Engenharia Biologica e Quimica, Instituto Superior
Tecnico, Lisbon 1046-001, Portugal
*
This work was supported in part by National Institutes of
Health Grant RO1 GM41840 (to D. J. T.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Burroughs Wellcome Toxicology Scholar. To whom correspondence
should be addressed. Tel.: 734-763-5717; Fax: 734-763-4581; E-mail:
dthiele@umich.edu.
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