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Abstract

The ability of to acquire iron from the hostile environment of the host is known to be necessary for virulence and appears to be achieved using a similar system to that described for . In , high-affinity iron uptake is dependent upon the acquisition of copper. The authors have previously identified a gene () that encodes a copper transporter. Deletion of this gene results in a mutant strain that grows predominantly as pseudohyphae and displays aberrant morphology in low-copper conditions. This paper demonstrates that invasive growth by is induced by low-copper conditions and that this is augmented in a -null strain. It also shows that deletion of results in defective iron uptake. In , genes that facilitate high-affinity copper uptake are controlled by a copper-sensing transactivator, Mac1p. The authors have now identified a gene () that encodes a copper-sensing transactivator. A -null mutant displays phenotypes similar to those of a -null mutant and has no detectable transcripts in low-copper conditions. It is proposed that high-affinity copper uptake by is necessary for reductive iron uptake and is transcriptionally controlled by Mac1p in a similar manner to that in .

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2004-07-01
2025-01-16
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