A mutant of Candida albicans deficient in beta-N-acetylglucosaminidase (chitobiase).
A mutant of Candida albicans ATCC 10261 was isolated that was defective in the production of beta-N-acetylglucosaminidase (chitobiase). The mutant grew normally in minimal medium supplemented with either glucose or N-acetyl-D-glucosamine (GlcNAc) as carbon and energy source, and the cells formed germ-tubes at 37 degrees C when induced to do so with GlcNAc. However, unlike the wild-type parent strain, the mutant strain did not utilize N,N'-diacetylchitobiose for growth. The mutant and parent strains had similar growth rates on glucose or GlcNAc, similar rates of uptake of these sugars and similar rates of 14C-labelled amino acid incorporation. The chitobiase mutant did, however, contain 53-85% more chitin than the wild-type strain. No reversion of the mutant phenotype was observed following induction of mitotic recombination with UV light, suggesting that the mutant allele (chi) was carried homozygously in the chitobiase-deficient mutant. Although the chitobiase-deficient mutant was pathogenic, it was not as virulent as the wild-type strain.
Jenkinson
H F
HF
Department of Oral Biology and Oral Pathology, University of Otago, Faculty of Dentistry, Dunedin, New Zealand.
Shepherd
M G
MG
D000117:Acetylglucosamine / Q000493:pharmacokinetics; D000118:Acetylglucosaminidase / Q000172:deficiency*; D002176:Candida albicans / Q000201:enzymology* / Q000472:pathogenicity; D002686:Chitin / Q000032:analysis; D005656:Fungal Proteins / Q000096:biosynthesis; D005947:Glucose / Q000493:pharmacokinetics; D006596:Hexosaminidases / Q000172:deficiency*; D009154:Mutation
D005656:Fungal Proteins; D002686:Chitin; D006596:Hexosaminidases; D000118:Acetylglucosaminidase; D005947:Glucose; D000117:Acetylglucosamine