@article{mbs:/content/journal/micro/10.1099/mic.0.27004-0, author = "Marvin, Marcus E. and Mason, Robert P. and Cashmore, Annette M.", title = "The CaCTR1 gene is required for high-affinity iron uptake and is transcriptionally controlled by a copper-sensing transactivator encoded by CaMAC1", journal= "Microbiology", year = "2004", volume = "150", number = "7", pages = "2197-2208", doi = "https://doi.org/10.1099/mic.0.27004-0", url = "https://www.microbiologyresearch.org/content/journal/micro/10.1099/mic.0.27004-0", publisher = "Microbiology Society", issn = "1465-2080", type = "Journal Article", keywords = "CuRE, copper-responsive element", keywords = "BCS, bathocuproinedisulphonic acid", keywords = "BPS, bathophenanthrolinedisulphonic acid", keywords = "PPD, p-phenylenediamine", abstract = "The ability of Candida albicans 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 Saccharomyces cerevisiae. In S. cerevisiae, high-affinity iron uptake is dependent upon the acquisition of copper. The authors have previously identified a C. albicans gene (CaCTR1) 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 C. albicans is induced by low-copper conditions and that this is augmented in a Cactr1-null strain. It also shows that deletion of CaCTR1 results in defective iron uptake. In S. cerevisiae, genes that facilitate high-affinity copper uptake are controlled by a copper-sensing transactivator, ScMac1p. The authors have now identified a C. albicans gene (CaMAC1) that encodes a copper-sensing transactivator. A Camac1-null mutant displays phenotypes similar to those of a Cactr1-null mutant and has no detectable CaCTR1 transcripts in low-copper conditions. It is proposed that high-affinity copper uptake by C. albicans is necessary for reductive iron uptake and is transcriptionally controlled by CaMac1p in a similar manner to that in S. cerevisiae.", }