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Gyanendra Tripathi,
Gwyneth Bertram,
Susan Macaskill,
Abigail Mavor,
Louise Walker,
Frank C. Odds,
Neil A. R. Gow, and
Alistair J. P. Brown*
Aberdeen Fungal Group, School of Medical Sciences, University of Aberdeen, Institute of Medical Sciences, Foresterhill, Aberdeen AB25 2ZD, United Kingdom
Received 10 May 2005/ Accepted 13 July 2005
The pathogen Candida albicans responds to amino acid starvation by activating pseudohyphal development and the expression of amino acid biosynthetic genes (GCN response). In Saccharomyces cerevisiae, the GCN response is dependent on Gcn2, which regulates the translation of the transcription factor Gcn4. Therefore, we examined the role of Gcn2 in C. albicans by using molecular, cellular, and genomic approaches. We show that C. albicans GCN2 encodes an eIF2
kinase, like its S. cerevisiae homologue. However, GCN4 appears to be regulated mainly at the transcriptional level in C. albicans. Furthermore, the inactivation of C. albicans Gcn2 only partially attenuates growth under amino acid starvation conditions and resistance to the histidine analogue 3-aminotriazole. Our comparison of the Gcn4 and Gcn2 regulons by transcript profiling reinforces the view that Gcn2 contributes to, but is not essential for, the activation of general amino acid control in C. albicans.
Present address: Flanders Interuniversity Institute for Biotechnology, Department of Molecular Microbiology, Katholieke Universiteit Leuven, B-3001 Leuven, Belgium.
Present address: The Babraham Institute, Babraham, Cambridge CB2 4AT, United Kingdom.
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