@article{mbs:/content/journal/micro/10.1099/00221287-133-8-2097, author = "JENKINSON, H. F. and SHEPHERD, M. G.", title = "A Mutant of Candida albicans Deficient in β-N-Acetylglucosaminidase (Chitobiase)", journal= "Microbiology", year = "1987", volume = "133", number = "8", pages = "2097-2106", doi = "https://doi.org/10.1099/00221287-133-8-2097", url = "https://www.microbiologyresearch.org/content/journal/micro/10.1099/00221287-133-8-2097", publisher = "Microbiology Society", issn = "1465-2080", type = "Journal Article", abstract = "SUMMARY: A mutant of Candida albicans ATCC 10261 was isolated that was defective in the production of β-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°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.", }