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Infect. Immun., Dec 1997, 4909-4917, Vol 65, No. 12
R Petter, YC Chang and KJ Kwon-Chung
The SNF1 gene of Saccharomyces cerevisiae (ScSNF1) is essential for the
derepression of catabolic repression. We report here the isolation and
characterization of an SNF1 homolog from Candida albicans (CaSNF1) which is
apparently essential for the viability of this organism. The putative amino
acid sequence of CaSNF1 has 68% identity with that of ScSNF1 and can
restore the S. cerevisiae snf1 delta mutant's ability to utilize sucrose.
Disruption of one of the CaSNF1 alleles resulted in morphological changes
and decreased growth rates but did not modify the carbon source utilization
pattern. Repetitive unsuccessful attempts to generate a snf1/snf1
homozygote by disruption of the second allele, using various vectors and
approaches, suggest the lethal nature of this mutation. Integration into
the second allele was possible only when a full-length functional SNF1
sequence was reassembled, further supporting this hypothesis and indicating
that the indispensability of Snf1p prevented the isolation of snf1/snf1
mutants. The mutant bearing two disrupted SNF1 alleles and the SNF1
functional sequence maintained its ability to utilize sucrose and produced
stellate colonies with extensive hyphal growth on agar media. It was
demonstrated that in a mouse model, the virulences of this mutant and the
wild-type strain are similar, suggesting that hyphal growth in vitro is not
an indicator for higher virulence.
Copyright © 1997, American Society for Microbiology
A gene homologous to Saccharomyces cerevisiae SNF1 appears to be essential for the viability of Candida albicans
Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892, USA.
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