Dominant suppressors of yeast actin mutations that are reciprocally suppressed.
Dominant suppressors of yeast actin mutations that are reciprocally suppressed.
复制标题
酵母肌动蛋白突变的显性抑制因子相互抑制。
DOI：
10.1093/genetics/121.4.675
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发表时间：
1989
期刊：
影响因子：
3.3
通讯作者：
Botstein,D
中科院分区：
文献类型：
--
作者：
Adams,AE;Botstein,D
一个基因，其产品很可能与酵母肌动蛋白相互作用的分离携带显性抑制剂的温度敏感性（Ts）act 1 -1突变的假回复突变体。在分析的30个独立回复突变体中，发现29个携带基因外抑制突变，其中24/24个检测的回复突变体相互关联。这个连锁群确定了一个新的基因SAC 6，其产品，由几个遗传标准，可能与肌动蛋白密切互动。首先，虽然act 1 -1 sac 6菌株是温度非依赖性的（Ts+），4/17的sac 6突变体等位基因测试是Ts在ACT 1+背景。此外，这些ACT 1 + sac 6突变体的4个Ts+假回复突变体携带ACT 1中的抑制突变;值得注意的是，其中3个在SAC 6+背景中再次是Ts，并且最有可能是新的ACT 1突变等位基因。因此，ACT 1和SAC 6的突变可以抑制彼此的缺陷。其次，sac 6突变可以抑制act 1 -1和act 1 -2的Ts缺陷，但不能抑制act 1 -4突变。这种等位基因特异性表明，sac 6突变并不通过简单地绕过肌动蛋白在高温下的功能来抑制。第三，act 1 -4 sac 6菌株的生长缺陷大于单独的单一突变，再次表明两种蛋白质之间的相互作用。根据act 1 -1 sac 6突变体文库中显性抑制的原理，克隆了突变体sac 6基因，并将其定位于第IV染色体上，距离ARO 1不到2 cM。
A gene whose product is likely to interact with yeast actin was identified by the isolation of pseudorevertants carrying dominant suppressors of the temperature-sensitive (Ts) act1-1 mutation. Of 30 independent revertants analyzed, 29 were found to carry extragenic suppressor mutations and of these, 24/24 tested were found to be linked to each other. This linkage group identifies a new gene SAC6, whose product, by several genetic criteria, is likely to interact intimately with actin. First, although act1-1 sac6 strains are temperature-independent (Ts+), 4/17 sac6 mutant alleles tested are Ts in an ACT1+ background. Moreover, four Ts+ pseudorevertants of these ACT1+ sac6 mutants carry suppressor mutations in ACT1; significantly, three of these are again Ts in a SAC6+ background, and are most likely new act1 mutant alleles. Thus, mutations in ACT1 and SAC6 can suppress each other's defects. Second, sac6 mutations can suppress the Ts defects of the act1-1 and act1-2, but not act1-4, mutations. This allele specificity indicates the sac6 mutations do not suppress by simply bypassing the function of actin at high temperature. Third, act1-4 sac6 strains have a growth defect greater than that due to either of the single mutations alone, again suggesting an interaction between the two proteins. The mutant sac6 gene was cloned on the basis of dominant suppression from an act1-1 sac6 mutant library, and was then mapped to chromosome IV, less than 2 cM from ARO1.