Takita M A, Castilho-Valavicius B
Department of Biochemistry, University of São Paulo, Brazil.
Yeast. 1993 Jun;9(6):589-98. doi: 10.1002/yea.320090605.
Kluyveromyces lactis killer toxin causes sensitive strains of a variety of yeasts to arrest at the G1 stage of the cell cycle, and to lose viability. We describe here the isolation and characterization of a class of recessive mutations in Saccharomyces cerevisiae that leads to toxin resistance and a temperature-sensitive phenotype. These mutant cells arrest growth at 37 degrees C with a characteristic phenotype of elongated buds. Cloning of the gene complementing these defects revealed it to be CAL1, coding for chitin synthase 3 activity. Calcofluor staining of the mutant cells indicated that chitin is absent both at 23 degrees C and 37 degrees C. Given that the CAL1 activity is responsible for the synthesis of most of chitin in yeast cells, and that in its absence the cells are viable but resistant to the killer toxin, our results strongly suggest that chitin might represent the receptor for this killer toxin.
乳酸克鲁维酵母杀伤毒素会使多种酵母的敏感菌株在细胞周期的G1期停滞，并丧失活力。我们在此描述了酿酒酵母中一类隐性突变的分离和特性，这些突变导致毒素抗性和温度敏感表型。这些突变细胞在37℃时停止生长，具有伸长芽的特征表型。对这些缺陷进行互补的基因克隆显示它是CAL1，编码几丁质合酶3活性。对突变细胞进行荧光增白剂染色表明，在23℃和37℃时均不存在几丁质。鉴于CAL1活性负责酵母细胞中大部分几丁质的合成，并且在其缺失时细胞仍可存活但对杀伤毒素具有抗性，我们的结果强烈表明几丁质可能是这种杀伤毒素的受体。
