A Mutant of Candida Albicans Deficient in beta-N-acetylglucosaminidase (Chitobiase)

J Gen Microbiol. 1987 Aug;133(8):2097-106. doi: 10.1099/00221287-133-8-2097.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylglucosamine / pharmacokinetics
  • Acetylglucosaminidase / deficiency*
  • Candida albicans / enzymology*
  • Candida albicans / pathogenicity
  • Chitin / analysis
  • Fungal Proteins / biosynthesis
  • Glucose / pharmacokinetics
  • Hexosaminidases / deficiency*
  • Mutation

Substances

  • Fungal Proteins
  • Chitin
  • Hexosaminidases
  • Acetylglucosaminidase
  • Glucose
  • Acetylglucosamine