Dagkesamanskaya A R, Ter-Avanesyan M D
Institute of Experimental Cardiology, USSR Cardiology Research Center, Moscow.
Genetics. 1991 Jul;128(3):513-20. doi: 10.1093/genetics/128.3.513.
The SUP1 and SUP2 genes code for protein factors intimately involved in the control of translational accuracy. The disrupted alleles of these genes confer a recessive lethal phenotype in both [psi+] and [psi-] genetic backgrounds, indicating an essential function for the corresponding proteins. In [psi+] diploids, heterozygous for the SUP1 null allele, several dominant phenotypes were evident with slow growth and inability to sporulate. These dominant phenotypes disappear after transformation with the multicopy plasmid carrying the wild-type allele of the SUP1 gene. Such dominant phenotypes were not observed for the SUP2 null allele. The incompatibility of multicopy plasmids carrying the SUP2 gene with guanidine hydrochloride-curable cytoplasmic factor(s) was also demonstrated. The possible mechanisms of interaction of the SUP1 and SUP2 genes with the [psi] determinant are discussed.
SUP1和SUP2基因编码与翻译准确性控制密切相关的蛋白质因子。这些基因的突变等位基因在[psi+]和[psi-]遗传背景中均呈现隐性致死表型，表明相应蛋白质具有重要功能。在[psi+]二倍体中，对于SUP1无效等位基因呈杂合状态，出现了几种显性表型，包括生长缓慢和无法形成孢子。用携带SUP1基因野生型等位基因的多拷贝质粒转化后，这些显性表型消失。对于SUP2无效等位基因，未观察到此类显性表型。还证明了携带SUP2基因的多拷贝质粒与盐酸胍可治愈的细胞质因子不兼容。讨论了SUP1和SUP2基因与[psi]决定因素相互作用的可能机制。
