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首页> 外文期刊>Molecular and Cellular Biology >Saccharomyces cerevisiae mutants unresponsive to alpha-factor pheromone: alpha-factor binding and extragenic suppression.
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Saccharomyces cerevisiae mutants unresponsive to alpha-factor pheromone: alpha-factor binding and extragenic suppression.

机译：酿酒酵母突变体对α-因子信息素无反应：α-因子结合和外源抑制。

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Mutations in six genes that eliminate responsiveness of Saccharomyces cerevisiae a cells to alpha-factor were examined by assaying the binding of radioactively labeled alpha-factor to determine whether their lack of responsiveness was due to the absence of alpha-factor receptors. The ste2 mutants, known to be defective in the structural gene for the receptor, were found to lack receptors when grown at the restrictive temperature; these mutations probably affect the assembly of active receptors. Mutations in STE12 known to block STE2 mRNA accumulation also resulted in an absence of receptors. Mutations in STE4, 5, 7, and 11 partially reduced the number of binding sites, but this reduction was not sufficient to explain the loss of responsiveness; the products of these genes appear to affect postreceptor steps of the response pathway. As a second method of distinguishing the roles of the various STE genes, we examined the sterile mutants for suppression. Mating of the ste2-3 mutant was apparently limited by its sensitivity to alpha-factor, as its sterility was suppressed by mutation sst2-1, which leads to enhanced alpha-factor sensitivity. Sterility resulting from each of four ste4 mutations was suppressed partially by mutation sst2-1 or by mutation bar1-1 when one of three other mutations (ros1-1, ros2-1, or ros3-1) was also present. Sterility of the ste5-3 mutant was suppressed by mutation ros1-1 but not by sst2-1. The ste7, 11, and 12 mutations were not suppressed by ros1 or sst2. Our working model is that STE genes control the response to alpha-factor at two distinct steps. Defects at one step (requiring the STE2 gene are suppressed (directly or indirectly) by mutation sst2-1, whereas defects at the other step (requiring the STE5 gene) are suppressed by the ros1-1 mutation. The ste4 mutants are defective for both steps. Mutation ros1-1 was found to be allelic to cdc39-1. Map positions for genes STE2, STE12, ROS3, and FUR1 were determined.
机译：通过测定放射性标记的α-因子的结合以确定其是否缺乏响应性，是由于缺少α-因子受体，检查了消除啤酒酵母细胞对α-因子的六个基因的突变。已知在受体的结构基因中有缺陷的ste2突变体，在限制温度下生长时缺乏受体。这些突变可能会影响活性受体的装配。已知可阻断STE2 mRNA积累的STE12突变也导致受体缺失。 STE4、5、7和11中的突变部分减少了结合位点的数量，但是这种减少不足以解释反应性的丧失。这些基因的产物似乎影响了反应途径的受体后步骤。作为区分各种STE基因作用的第二种方法，我们检查了无菌突变体的抑制作用。 ste2-3突变体的交配显然受到其对α因子的敏感性的限制，因为其不育性被突变sst2-1抑制，这导致增强的α因子敏感性。当同时存在其他三个突变中的一个（ros1-1，ros2-1或ros3-1）之一时，由sst2-1突变或bar1-1突变会部分抑制由四个ste4突变中的每一个引起的不育。 ste5-3突变体的不育性受到ros1-1突变的抑制，而不受sst2-1突变的抑制。 ros1或sst2不能抑制ste7、11和12突变。我们的工作模型是STE基因在两个不同的步骤控制对α因子的反应。一步sst2-1抑制了（直接或间接）一步的缺陷（需要STE2基因），而ros1-1突变抑制了另一步的缺陷（需要STE5基因）。步骤：发现ros1-1突变与cdc39-1等位基因，确定了STE2，STE12，ROS3和FUR1基因的图谱位置。

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