1887

Abstract

Copper and iron uptake in are linked through a high-affinity ferric/cupric-reductive uptake system. Evidence suggests that a similar system operates in . The authors have identified a gene that is able to rescue a /-null mutant defective in high-affinity copper uptake. The 756 bp ORF, designated , encodes a 251 amino acid protein with a molecular mass of 27·8 kDa. Comparisons between the deduced amino acid sequence of the Ctr1p and Ctr1p indicated that they share 39·6 % similarity and 33·0 % identity over their entire length. Within the predicted protein product of there are putative transmembrane regions and sequences that resemble copper-binding motifs. The promoter region of contains four sequences with significant identity to copper response elements. is transcriptionally regulated in in response to copper availability by the copper-sensing transactivator Mac1p. Transcription of in is also regulated in a copper-responsive manner. This raises the possibility that may be regulated in by a Mac1p-like transactivator. A -null mutant displays phenotypes consistent with the lack of copper uptake including growth defects in low-copper and low-iron conditions, a respiratory deficiency and sensitivity to oxidative stress. Furthermore, changes in morphology were observed in the -null mutant. It is proposed that facilitates transport of copper into the cell.

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2003-06-01
2024-04-25
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