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第 7 期:绿藻莱茵衣藻中钼喋呤辅酶生物合成的新基因座。

nit 7: A New Locus for Molybdopterin Cofactor Biosynthesis in the Green Alga Chlamydomonas reinhardtii.

机构信息

Departamento de Bioquímica y Biología Molecular y Fisiología, Avda. San Alberto Magno s/n, Universidad de Córdoba, 14071-Córdoba, Spain.

出版信息

Plant Physiol. 1992 Jan;98(1):395-8. doi: 10.1104/pp.98.1.395.

Abstract

Two new nitrate reductase-deficient mutants from Chlamydomonas reinhardtii have been genetically and biochemically characterized. Both H1 and F23 mutants carry single recessive allelic mutations that map at a new locus designated nit-7. This locus is unlinked to the other six nit loci related to the nitrate assimilation pathway in C. reinhardtii. Both mutant alleles H1 and F23 lack an active molybdopterin cofactor, the activity of which is restored neither in vitro nor in vivo by high concentrations of molybdate. Nitrate reductase subunits in these mutants seem to assemble, although not in a stable form, in a high molecular weight complex and, as in other molybdenum cofactor-defective mutants of C. reinhardtii, they cannot reconstitute nitrate reductase activity with an active molybdenum cofactor source from extracts of ammonium-grown cells. The results suggest that nit-7 mutants are defective in molybdopterin biosynthesis. They do produce some precursor(s) that are capable of binding to nitrate reductase subunits.

摘要

两个来自莱茵衣藻的硝酸还原酶缺陷突变体已被从遗传学和生物化学方面进行了特征描述。突变体 H1 和 F23 均携带单个隐性等位基因突变,这些突变基因定位于一个新的被命名为 nit-7 的基因座上。该基因座与其他六个与硝酸盐同化途径有关的 nit 基因座在莱茵衣藻中没有关联。两个突变等位基因 H1 和 F23 都缺乏活性的钼喋呤辅因子,高浓度的钼酸盐既不能在体外也不能在体内恢复其活性。这些突变体中的硝酸还原酶亚基似乎组装成一个高分子量的复合物,尽管不是稳定的形式,而且与莱茵衣藻的其他钼辅因子缺陷突变体一样,它们不能用来自铵培养细胞提取物中的活性钼辅因子来源重新构成硝酸还原酶活性。结果表明,nit-7 突变体在钼喋呤生物合成中存在缺陷。它们确实产生了一些能够与硝酸还原酶亚基结合的前体。

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