Regulation of genes controlling synthesis of the galactose pathway enzymes in yeast.
Regulation of genes controlling synthesis of the galactose pathway enzymes in yeast.
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控制酵母中半乳糖途径酶合成的基因的调节。
DOI：
10.1093/genetics/54.3.911
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发表时间：
1966
期刊：
影响因子：
3.3
通讯作者：
D. Hawthorne
中科院分区：
文献类型：
--
作者：
H. C. Douglas;D. Hawthorne
酿酒酵母菌半乳糖途径酶合成的遗传控制在某些方面符合JACOB和MONOD（1961）提出的大肠杆菌半乳糖苷酶系统的操纵子模型，BUTTIN （1963a, b）也证明该模型适用于大肠杆菌半乳糖系统。三个紧密相连的结构基因指定了半乳糖途径酶，半乳糖激酶，半乳糖-1-磷酸-尿苷基转移酶（转移酶）和尿苷二磷酸半乳糖-4-epimerase (epimerase) （DOUGLAS和HAWTHORNE 1964）。这三个位点受一个非连锁调节基因i的控制，该基因可通过其隐性突变识别，该突变允许三种半乳糖酶的组成合成（DOUGLAS and PELROY 1963）。细菌系统的一个关键特征，在酵母系统中似乎不存在，即操作基因与结构基因的密切联系（DOUGLAS和HAWTHORNE， 1964）。操作基因座最初被定义为与结构基因相连的区域，其中发生两种类型的突变：O ‘ ‘，其表达为顺式显性，用于操纵子蛋白的组成性合成，而Oo ’ ’则阻止操纵子所有蛋白质的合成。JACOB和MONOD（1965）重新定义了大肠杆菌p-半乳糖苷酶系统中的操作位点，即0”突变识别阻遏物的位点。该系统中的0”突变现在被认为是操纵子第一个结构基因的极性突变（BECKWITH 1964）。酵母中导致三种半乳糖酶合成失败的突变，因此类似于Oo型的表型突变，可以很容易地分离出来。然而，这些不是极性突变体，也不是诱导剂摄取或代谢缺陷的突变体。它们位于GA位点，该位点独立于半乳糖结构基因分离，并且它们的表型与i结合时不变（DOUGLAS和HAWTHORNE， 1964）。酵母半乳糖系统中显示显性组成表型的突变的发生以及这些突变与GA、区域和半乳糖酶结构基因的关系是本论文的主题。
HE genetic control of synthesis of the galactose pathway enzymes in Saccharomyces cerevisiae conforms in certain respects to the operon model proposed by JACOB and MONOD (1961) for the ,&galactosidase system of E. coli, and shown by BUTTIN (1963a, b) to be valid for the E. coli galactose system as well. Three closely linked structural genes specify the galactose pathway enzymes, galactokinase, galactose-1-phosphate-uridyl transferase (transferase), and uridine diphosphogalactose-4-epimerase (epimerase) (DOUGLAS and HAWTHORNE 1964). The three loci are under the control of an unlinked regulator gene, i, which is recognizable by its recessive mutations that permit constitutive synthesis of the three galactose enzymes (DOUGLAS and PELROY 1963). A key feature of the bacterial systems which appears to be absent in the yeast system in the close association of an operator gene with the structural genes (DOUGLAS and HAWTHORNE 1964). The operator locus was defined originally as a region linked to the structural genes in which two types of mutations occurred: O", which were expressed as cis-dominant for constitutive synthesis of the operon proteins, and Oo, which prevented synthesis of all of the proteins of the operon. JACOB and MONOD (1965) have redefined the operator locus in the p-galactosidase system of E. coli as the site of repressor recognition identified by 0" mutations. The 0" mutations in this system are now considered to be polarity mutations within the first structural gene of the operon (BECKWITH 1964). Mutations in yeast that result in failure to synthesize the three galactose enzymes and thus resemble phenotypically mutations of the Oo type can be readily isolated. However, these are not polarity mutants nor are they mutants in which inducer uptake or metabolism is defective. They map in the GA, locus which segregates independently of the galactose structural genes and their phenotype is unchanged in combination with i(DOUGLAS and HAWTHORNE 1964). The occurrence of mutations in the yeast galactose system which display the dominant constitutive phenotype and the relationship of these mutants to the GA, region and to the structural genes for the galactose enzymes is the subject of the present paper.