Killer-toxin-resistant kre12 mutants of Saccharomyces cerevisiae : genetic and biochemical evidence for a secondary K1 membrane receptor

1995 ◽  
Vol 164 (6) ◽  
pp. 435-443 ◽  
Author(s):  
M. J. Schmitt ◽  
Pascal Compain
1990 ◽  
Vol 265 (28) ◽  
pp. 17274-17280
Author(s):  
M Tokunaga ◽  
A Kawamura ◽  
K Kitada ◽  
F Hishinuma

1985 ◽  
Vol 31 (3) ◽  
pp. 300-302 ◽  
Author(s):  
Gianfranco Rosini

The cross-reaction between 6 killer strains of Saccharomyces cerevisiae and 41 killer strains of Hansenula anomala var. anomala was examined. Fifteen strains of Hansenula killed one or more cultures of S. cerevisiae. None of the killer strains of H. anomala var. anomala was killed by S. cerevisiae killer strains or by killer strains of the same species. In S. cerevisiae different killer toxin and immunity systems were represented. Intraspecific killing activity was not found among the 41 strains of H. anomala var. anomala.


1987 ◽  
Vol 50 (3) ◽  
pp. 234-238 ◽  
Author(s):  
FERDINAND RADLER ◽  
MANFRED SCHMITT

The killer toxin (KT 28), a glycoprotein of Saccharomyces cerevisiae strain 28, was almost completely adsorbed by bentonite, when applied at a concentration of 1 g per liter. No significant differences were found between several types of bentonite. Killer toxin KT 28 is similarly adsorbed by intact yeast cells or by a commercial preparation of yeast cell walls that has been recommended to prevent stuck fermentations. An investigation of the cell wall fractions revealed that the toxin KT 28 was mainly adsorbed by mannan, that removed the toxin completely. The alkali-soluble and the alkali-insoluble β-1,3- and β-1,6-D-glucans lowered the toxin concentration to one tenth of the original amount. The killer toxin of the type K1 of S. cerevisiae was adsorbed much better by glucans than by mannan.


1998 ◽  
Vol 180 (19) ◽  
pp. 5020-5029 ◽  
Author(s):  
Shigehisa Nagahashi ◽  
Marc Lussier ◽  
Howard Bussey

ABSTRACT The Candida glabrata KRE9 (CgKRE9) andKNH1 (CgKNH1) genes have been isolated as multicopy suppressors of the tetracycline-sensitive growth of aSaccharomyces cerevisiae mutant with the disruptedKNH1 locus and the KRE9 gene placed under the control of a tetracycline-responsive promoter. Although acgknh1Δ mutant showed no phenotype beyond slightly increased sensitivity to the K1 killer toxin, disruption ofCgKRE9 resulted in several phenotypes similar to those of the S. cerevisiae kre9Δ null mutant: a severe growth defect on glucose medium, resistance to the K1 killer toxin, a 50% reduction of β-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 cgknh1Δbackground rendered cell growth tetracycline sensitive on media containing glucose or galactose. cgkre9Δ 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.


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