Control of yeast cell type by the mating type locus. I. Identification and control of expression of the a-specific gene BAR1.
Control of yeast cell type by the mating type locus. I. Identification and control of expression of the a-specific gene BAR1.
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通过交配型基因座控制酵母细胞类型。
DOI：
10.1016/0022-2836(81)90280-1
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发表时间：
1981
影响因子：
5.6
通讯作者：
Herskowitz,I
中科院分区：
文献类型：
--
作者：
SpragueJr,GF;Herskowitz,I
酵母交配型基因座的MATα等位基因具有α交配表型，包含MATα1和MATα2两个互补基团。α1-α2假说认为MATα1是α特异基因的正调节因子，MATα2是α特异基因的负调节因子。根据这一假设，MATα2突变体在交配和产生胞外α因子方面存在缺陷，表现出博塔特异功能(因为它们缺乏MATα2产物)和α特异功能(因为它们含有MATα1产物)。未能产生细胞外α因子是由于这些功能之间的拮抗；特别是因为α因子(一种α特有的功能)被a特有的功能降解。如果这一观点是正确的，MATα2突变体应该获得产生α因子的能力，如果他们也携带负责α因子降解的基因(S)的缺陷。我们已经分离到一个产生α-因子的AMATα-2突变体的衍生物，并对该菌株中的抑制突变进行了鉴定。(1)该菌株携带与HIS6紧密连锁的突变(Bar1-1)(位于第九染色体上)，允许α2突变株产生α因子。(2)不允许MATα-1突变体产生α-因子。(3)携带Bar1-1突变的交配型单倍体仍然交配，但不能作为α因子扩散的屏障。Matabar1-1细胞对α因子的敏感性增加。(4)引起对−-因子敏感性增加的突变(sst1-α-2)是α-1-1的等位基因，也允许通过α-2突变体合成sst1-因子。MATα2bar1双突变体产生胞外α因子的能力表明MATα2突变体确实产生α因子，但它被屏障功能降解。这些结果表明，BAR1只在a细胞中正常表达，并且在α细胞中受α2产物的负调控。
TheMATα allele of the yeast mating type locus confers the α mating phenotype and contains two complementation groups,MATα1 andMATα2. The α1–α2 hypothesis proposes thatMATα1 is a positive regulator of α-specific genes and thatMATα2 is a negative regulator of a-specific genes. According to this hypothesis,matα2 mutants, which are defective in mating and in production of extracellular α-factor, expressbotha-specific functions (because they lackMATα2 product) and α-specific functions (because they containMATα1 product). Failure to produce extracellular α-factor results from antagonism between these functions; in particular, because α-factor (an α-specific function) is degraded by an a-specific function. If this view is correct,matα2 mutants should acquire the ability to produce α-factor if they also carry a defect in the gene(s) responsible for α-factor degradation. We have isolated a derivative of amatα2 mutant that produces α-factor and have characterized the suppressor mutation in this strain. (1) This strain carries a mutation (bar1-1) tightly linked toHIS6 (on chromosome IX) that allowsmatα2 mutants to produce α-factor. (2) It does not allowmatα1 mutants to produce α-factor. (3) Haploids of the a mating type bearing thebar1-1 mutation still mate, but are unable to act as a barrier to the diffusion of α-factor.MATabar1-1 cells display increased sensitivity to α-factor. (4) A mutation (sst1−2) that causes increased sensitivity to α-factor is allelic tobar1-1 and also allows α-factor synthesis bymatα2 mutants. The ability ofmatα2bar1 double mutants to produce extracellular α-factor indicates thatmatα2 mutants do produce α-factor but that it is degraded by the Barrier function. These results suggest thatBAR1 is normally expressed only in a cells, and is negatively regulated in α cells by theMATα2 product.
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作者：
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DOI：
10.1136/jnnp.43.10.861
发表时间：
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期刊：
Journal of Neurology, Neurosurgery & Psychiatry
影响因子：
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