抗嘌呤的黑腹果蝇是由腺嘌呤磷酸核糖转移酶结构基因突变产生的。

Purine-resistant Drosophila melanogaster result from mutations in the adenine phosphoribosyltransferase structural gene.

作者信息

Johnson D H, Friedman T B

出版信息

Proc Natl Acad Sci U S A. 1983 May;80(10):2990-4. doi: 10.1073/pnas.80.10.2990.

DOI:10.1073/pnas.80.10.2990

PMID:6407004

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC393959/

Abstract

Mutants of Drosophila melanogaster selected for resistance to purine killing are deficient in adenine phosphoribosyltransferase (APRT; E.C. 2.4.2.7) activity. Genetic mapping and complementation analysis demonstrate that purine resistance, deficiency of APRT activity, and differences in the isoelectric point of APRT result from alterations at a single locus, Aprt (map position, 3:3.03). The level of APRT activity shows gene dose dependence in Aprt heterozygotes and in flies that are haploid for different Aprt alleles. Drosophila APRT is a dimer composed of apparently identical 23,000-dalton subunits. These results suggest that Aprt contains the structural gene for APRT.

摘要

为抗嘌呤杀伤而选择的黑腹果蝇突变体，其腺嘌呤磷酸核糖转移酶（APRT；E.C. 2.4.2.7）活性存在缺陷。遗传图谱绘制和互补分析表明，嘌呤抗性、APRT活性缺陷以及APRT等电点的差异是由单个基因座Aprt（图谱位置，3:3.03）的改变所致。在Aprt杂合子以及不同Aprt等位基因单倍体的果蝇中，APRT活性水平呈现基因剂量依赖性。果蝇APRT是一种由明显相同的23,000道尔顿亚基组成的二聚体。这些结果表明，Aprt包含APRT的结构基因。