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Journal of Bacteriology, October 1998, p. 5020-5029, Vol. 180, No. 19
Department of Biology, McGill University,
Montréal, Quebec, Canada H3A 1B1
Received 18 May 1998/Accepted 28 July 1998
The Candida glabrata KRE9 (CgKRE9) and
KNH1 (CgKNH1) genes have been isolated as
multicopy suppressors of the tetracycline-sensitive growth of a
Saccharomyces cerevisiae mutant with the disrupted KNH1 locus and the KRE9 gene placed under the
control of a tetracycline-responsive promoter. Although a
cgknh1
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Isolation of Candida glabrata Homologs
of the Saccharomyces cerevisiae KRE9 and KNH1
Genes and Their Involvement in Cell Wall
-1,6-Glucan
Synthesis

mutant showed no phenotype beyond slightly
increased sensitivity to the K1 killer toxin, disruption of
CgKRE9 resulted in several phenotypes similar to those of
the S. cerevisiae kre9
null mutant: a severe growth
defect on glucose medium, resistance to the K1 killer toxin, a 50%
reduction of
-1,6-glucan, and the presence of aggregates of cells
with abnormal morphology on glucose medium. Replacement in C. glabrata of the cognate CgKRE9 promoter with
the tetracycline-responsive promoter in a cgknh1
background rendered cell growth tetracycline sensitive on
media containing glucose or galactose. cgkre9
cells were
shown to be sensitive to calcofluor white specifically on glucose
medium. In cgkre9 mutants grown on glucose medium, cellular
chitin levels were massively increased.
*
Corresponding author. Mailing address: Department of
Biology, McGill University, 1205 Dr. Penfield Ave., Montréal,
Quebec, Canada H3A 1B1. Phone: (514) 398-6439. Fax: (514)
398-2595. E-mail: hbussey{at}monod.biol.mcgill.ca.
Present address: Department of Mycology, Nippon Roche Research
Center, Kamakura, Kanagawa 247-8530, Japan.
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