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粗糙脉孢菌中黄嘌呤脱氢酶的表达不需要功能性的nit-2调控基因。

Xanthine dehydrogenase expression in Neurospora crassa does not require a functional nit-2 regulatory gene.

作者信息

Griffith A B, Garrett R H

机构信息

Department of Biology, University of Virginia, Charlottesville 22901.

出版信息

Biochem Genet. 1988 Feb;26(1-2):37-52. doi: 10.1007/BF00555487.

Abstract

Xanthine dehydrogenase (XDH) is the initial enzyme in the purine catabolic pathway of N. crassa. Secondary nitrogen sources such as purines are metabolized when preferred sources of reduced nitrogen (ammonium or glutamine) are unavailable. XDH synthesis is regulated by glutamine repression and uric acid induction. The nit-2 locus is believed to encode a trans-acting positive regulator essential for the expression of genes encoding enzymes involved in secondary pathways of nitrogen acquisition, such as XDH and nitrate reductase. However, immunoblot analyses and enzyme assays reveal that XDH protein is synthesized and XDH activity is expressed in nit-2 mutants. Nevertheless, XDH responds to nitrogen metabolite repression. The generality that nit-2 is an obligate control element in nitrogen metabolite repression is questioned. Additionally, mutants defective in XDH activity, namely, xdh-1 and the molybdenum cofactor mutants nit-1, -7, -8 and -9, are observed to grow on xanthine but not hypoxanthine.

摘要

黄嘌呤脱氢酶(XDH)是粗糙脉孢菌嘌呤分解代谢途径中的起始酶。当缺乏还原态氮的首选来源(铵或谷氨酰胺)时,诸如嘌呤等次要氮源会被代谢。XDH的合成受谷氨酰胺阻遏和尿酸诱导的调节。nit-2基因座被认为编码一种反式作用的正调控因子,对于参与氮获取次要途径的酶(如XDH和硝酸还原酶)的基因表达至关重要。然而,免疫印迹分析和酶活性测定表明,XDH蛋白在nit-2突变体中能够合成,且XDH活性也能表达。尽管如此,XDH对氮代谢物阻遏有反应。nit-2是氮代谢物阻遏中必不可少的控制元件这一普遍观点受到质疑。此外,观察到XDH活性缺陷的突变体,即xdh-1以及钼辅因子突变体nit-1、-7、-8和-9,能在黄嘌呤上生长,但不能在次黄嘌呤上生长。

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