Zahner J E, Harkins H A, Pringle J R
Department of Biology, University of North Carolina, Chapel Hill, 27599, USA.
Mol Cell Biol. 1996 Apr;16(4):1857-70. doi: 10.1128/MCB.16.4.1857.
Previous analysis of the bipolar budding pattern of Saccharomyces cerevisiae has suggested that it depends on persistent positional signals that mark the region of the division site and the tip of the distal pole on a newborn daughter cell, as well as each previous division site on a mother cell. In an attempt to identify genes encoding components of these signals or proteins involved in positioning or responding to them, we identified 11 mutants with defects in bipolar but not in axial budding. Five mutants displaying a bipolar budding-specific randomization of budding pattern had mutations in four previously known genes (BUD2, BUD5, SPA2, and BNI1) and one novel gene (BUD6), respectively. As Bud2p and Bud5p are known to be required for both the axial and bipolar budding patterns, the alleles identified here probably encode proteins that have lost their ability to interact with the bipolar positional signals but have retained their ability to interact with the distinct positional signal used in axial budding. The function of Spa2p is not known, but previous work has shown that its intracellular localization is similar to that postulated for the bipolar positional signals. BNI1 was originally identified on the basis of genetic interaction with CDC12, which encodes one of the neck-filament-associated septin proteins, suggesting that these proteins may be involved in positioning the bipolar signals. One mutant with a heterogeneous budding pattern defines a second novel gene (BUD7). Two mutants budding almost exclusively from the proximal pole carry mutations in a fourth novel gene (BUD9). A bud8 bud9 double mutant also buds almost exclusively from the proximal pole, suggesting that Bud9p is involved in positioning the proximal pole signal rather than being itself a component of this signal.
先前对酿酒酵母双极出芽模式的分析表明，它依赖于持续的位置信号，这些信号标记了分裂位点区域、新生子细胞远端极的顶端以及母细胞上的每个先前分裂位点。为了鉴定编码这些信号成分或参与定位或响应这些信号的蛋白质的基因，我们鉴定出了11个在双极出芽而非轴向出芽方面存在缺陷的突变体。五个表现出双极出芽特异性出芽模式随机化的突变体，分别在四个先前已知的基因（BUD2、BUD5、SPA2和BNI1）和一个新基因（BUD6）中发生了突变。由于已知Bud2p和Bud5p是轴向和双极出芽模式所必需的，这里鉴定出的等位基因可能编码的蛋白质已经失去了与双极位置信号相互作用的能力，但保留了与轴向出芽中使用的不同位置信号相互作用的能力。Spa2p的功能尚不清楚，但先前的研究表明其细胞内定位与双极位置信号的推测定位相似。BNI1最初是基于与CDC12的遗传相互作用而鉴定出来的，CDC12编码一种与颈部细丝相关的septin蛋白，这表明这些蛋白质可能参与双极信号的定位。一个具有异质出芽模式的突变体定义了第二个新基因（BUD7）。两个几乎完全从近端极出芽的突变体在第四个新基因（BUD9）中携带突变。bud8 bud9双突变体也几乎完全从近端极出芽，这表明Bud9p参与近端极信号的定位，而不是其本身就是该信号的一个成分。
