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[破坏黑腹果蝇6-磷酸葡萄糖酸脱氢酶形成的突变的性质及其抑制作用]

[Nature of mutations disrupting the formation of 6-phosphogluconate dehydrogenase in Drosophila melanogaster, and their suppression].

作者信息

Gvozdev V A, Gerasimova T I, Kogan G L, Rozovskiĭ Ia M

出版信息

Mol Biol (Mosk). 1977 Nov-Dec;11(6):1402-13.

PMID:88009
Abstract

Molecular nature of lethal and semilethal mutations in the Pgd locus of D. melanogaster coding for 6-phosphogluconate dehydrogenase (6tpgd) was studied. All these mutations affect the structural gene of the Pgd locus: 3 semilethal mutations resulted in altered 6PGD molecules with the decreased catalytic activity; the remaining 8 lethals were "zero" alleles possessing mutant polypeptides inactive but capable to react with antisera against highly purified 6PGD. "Zero" or low activity alleles for glucose-6-phosphate dehydrogenase induced by ethyl methansulfonate were shown to be supressors for the lethal mutations in the Pgd locus. A monocistronic type of organization of the Pgd locus is suggested taking into account the biochemical mechanism of supression of the Pgd-lethals and their location in the structural gene coding for 6GPD.

摘要

对果蝇编码6-磷酸葡萄糖酸脱氢酶(6PGD)的Pgd基因座中致死和半致死突变的分子性质进行了研究。所有这些突变都影响Pgd基因座的结构基因:3个半致死突变导致6PGD分子发生改变,催化活性降低;其余8个致死突变是“零”等位基因,其突变多肽无活性,但能够与针对高度纯化的6PGD的抗血清发生反应。甲磺酸乙酯诱导的葡萄糖-6-磷酸脱氢酶的“零”或低活性等位基因被证明是Pgd基因座中致死突变的抑制因子。考虑到Pgd致死突变的抑制生化机制及其在编码6GPD的结构基因中的位置,推测Pgd基因座为单顺反子类型的组织形式。

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