Brown J L, Kossaczka Z, Jiang B, Bussey H
Biology Department, McGill University, Montreal, Quebec, Canada.
Genetics. 1993 Apr;133(4):837-49. doi: 10.1093/genetics/133.4.837.
Recessive mutations leading to killer resistance identify the KRE9, KRE10 and KRE11 genes. Mutations in both the KRE9 and KRE11 genes lead to reduced levels of (1-->6)-beta-glucan in the yeast cell wall. The KRE11 gene encodes a putative 63-kD cytoplasmic protein, and disruption of the KRE11 locus leads to a 50% reduced level of cell wall (1-->6)-glucan. Structural analysis of the (1-->6)-beta-glucan remaining in a kre11 mutant indicates a polymer smaller in size than wild type, but containing a similar proportion of (1-->6)- and (1-->3)-linkages. Genetic interactions among cells harboring mutations at the KRE11, KRE6 and KRE1 loci indicate lethality of kre11 kre6 double mutants and that kre11 is epistatic to kre1, with both gene products required to produce the mature glucan polymer at wild-type levels. Analysis of these KRE genes should extend knowledge of the beta-glucan biosynthetic pathway, and of cell wall synthesis in yeast.
导致杀手抗性的隐性突变鉴定出了KRE9、KRE10和KRE11基因。KRE9和KRE11基因的突变都会导致酵母细胞壁中（1→6）-β-葡聚糖水平降低。KRE11基因编码一种推定的63-kD细胞质蛋白，破坏KRE11基因座会导致细胞壁（1→6）-葡聚糖水平降低50%。对kre11突变体中剩余的（1→6）-β-葡聚糖进行结构分析表明，其聚合物尺寸比野生型小，但（1→6）-和（1→3）-连接的比例相似。在KRE11、KRE6和KRE1基因座处携带突变的细胞之间的遗传相互作用表明，kre11 kre6双突变体具有致死性，并且kre11对kre1是上位性的，两种基因产物都需要以野生型水平产生成熟的葡聚糖聚合物。对这些KRE基因的分析应能扩展对β-葡聚糖生物合成途径以及酵母细胞壁合成的认识。
