Penn M D, Galgoci B, Greer H
Proc Natl Acad Sci U S A. 1983 May;80(9):2704-8. doi: 10.1073/pnas.80.9.2704.
In yeast, most amino acid biosynthetic pathways are coregulated: starvation for a single amino acid results in derepression of enzyme activities for many different biosynthetic pathways. This phenomenon is referred to as "general control of amino acid biosynthesis." In this paper we describe the isolation and characterization of 43 amino acid analog-sensitive (aas-) mutants that are perturbed in this general regulatory system. These 43 mutations define four unlinked complementation groups, AAS101, AAS102, AAS103, and AAS104, two of which identify previously unreported genes involved in general control. These aas mutants are unable to derepress a number of amino acid biosynthetic genes, resulting in increased sensitivity to amino acid analogs, reduced growth rates, and reduced enzyme activity levels under amino acid starvation conditions. Thus, the AAS+ gene products function as positive regulatory elements for this system. We show that the AAS genes mediate these effects by regulating the mRNA levels of genes under their control.
在酵母中,大多数氨基酸生物合成途径是共同调控的:单一氨基酸饥饿会导致许多不同生物合成途径的酶活性去阻遏。这种现象被称为“氨基酸生物合成的全局调控”。在本文中,我们描述了43个在这个全局调控系统中受到干扰的氨基酸类似物敏感(aas-)突变体的分离和特性。这43个突变定义了四个不连锁的互补群,AAS101、AAS102、AAS103和AAS104,其中两个鉴定出了以前未报道的参与全局调控的基因。这些aas突变体无法去阻遏许多氨基酸生物合成基因,导致对氨基酸类似物的敏感性增加、生长速率降低以及在氨基酸饥饿条件下酶活性水平降低。因此,AAS+基因产物作为该系统的正调控元件发挥作用。我们表明,AAS基因通过调节其控制下基因的mRNA水平来介导这些效应。