Isolation and characterisation of ferric reductase genes from the pathogenic yeast Candida albicans

Iron uptake in C. albicans has not been extensively studied to date, but the ferric reductase activity identified in our laboratory has been shown to be regulated in a similar manner to that of Saccharomyces cerevisiae, suggesting that the S. cerevisiae system provides a good model for iron uptake i...

Full description

Bibliographic Details
Main Author: Hammacott, Jane Elizabeth
Published: University of Leicester 2000
Subjects:
572
Online Access:http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.696822
Description
Summary:Iron uptake in C. albicans has not been extensively studied to date, but the ferric reductase activity identified in our laboratory has been shown to be regulated in a similar manner to that of Saccharomyces cerevisiae, suggesting that the S. cerevisiae system provides a good model for iron uptake in C. albicans. This study was identified two C. albicans ferric reductase genes, which are capable of rescuing a S. cerevisiae mutant defective in a structural ferric reductase gene, FRE1. Both genes, CFL1 (Candida ferric reductase like gene) and CFL2, encode proteins that show significant sequence identity with known ferric reductase proteins. Northern blot analysis has shown that CFL1 is negatively regulated by both iron and copper but CFL2 was not expressed under the conditions tested. Northern blot analysis has also been carried out on 6 other ferric reductase-like genes, which were identified through analysis of the C. albicans genome sequencing project (http://alces. med.umn.edu/Candida.html). Only one of these genes, CFL95, was shown to be expressed under the conditions tested and this gene was also negatively regulated by iron and copper. A C. albicans strain in which CFL1 has been deleted has been constructed and phenotypic tests on this mutant have shown that it still possesses a cell surface ferric reductase activity indistinguishable from wild type as well as still being able to grow in low iron conditions. This suggests that it may be an intracellular reductase or that the effects of deleting this gene may be masked by the presence of other ferric reductase-like genes, which may have redundant function.