Novotná Drahomíra, Flegelová Hana, Janderová Blanka
Department of Genetics and Microbiology, Faculty of Science, Charles University, Vinicná 5, 128 44, Prague 2, Czech Republic.
FEMS Yeast Res. 2004 Sep;4(8):803-13. doi: 10.1016/j.femsyr.2004.04.007.
Study of Saccharomyces cerevisiae killer toxin-sensitive strains with the deltakre2 phenotype (resistant to toxin K1, sensitive to toxin K2) showed that the phenotype is complemented by the KRE2 gene not only in intact cells but also in spheroplasts, and resistance to K1 thus resides very probably in the plasma membrane. deltakre1 deletant displays a faulty interaction with both K1 and K2 toxin. Hence, Kre1p probably serves as plasma membrane receptor for both toxins. Deletants in seven other genes (GDA1, SAC1, LUV1, KRE23, SAC2, KRE21, ERG4) exhibit different degrees of the deltakre2-like resistance pattern, but the phenotype in deltagda1 and deltasac1 is not connected with a defect in K1 toxin interaction with the plasma membrane, similarly as in deltakre6 and deltakre11 strains with a higher resistance to K2 toxin. Differences between the K1 and K2 killer toxin thus occur on the level of both the plasma membrane and the cell wall.
对具有δkre2表型(对毒素K1有抗性,对毒素K2敏感)的酿酒酵母杀伤毒素敏感菌株的研究表明,该表型不仅在完整细胞中,而且在原生质体中都能被KRE2基因互补,因此对K1的抗性很可能存在于质膜中。δkre1缺失体与K1和K2毒素都表现出错误的相互作用。因此,Kre1p可能是这两种毒素的质膜受体。其他七个基因(GDA1、SAC1、LUV1、KRE23、SAC2、KRE21、ERG4)的缺失体表现出不同程度的类似δkre2的抗性模式,但δgda1和δsac1中的表型与K1毒素与质膜相互作用的缺陷无关,这与对K2毒素具有较高抗性的δkre6和δkre11菌株类似。因此,K1和K2杀伤毒素之间的差异发生在质膜和细胞壁水平上。