SUMMARY: A mutant of ATCC 10261 was isolated that was defective in the production of β--acetylglucosaminidase (chitobiase). The mutant grew normally in minimal medium supplemented with either glucose or -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 '-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 C-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 () 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.


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