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铵、L-谷氨酸和L-谷氨酰胺对构巢曲霉氮分解代谢的影响。

Effects of ammonium, L-glutamate, and L-glutamine on nitrogen catabolism in Aspergillus nidulans.

作者信息

Hynes M J

出版信息

J Bacteriol. 1974 Dec;120(3):1116-23. doi: 10.1128/jb.120.3.1116-1123.1974.

DOI:10.1128/jb.120.3.1116-1123.1974
PMID:4612004
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC245890/
Abstract

During growth of Aspergillus nidulans in medium containing ammonium the specific activities of most enzymes involved in catabolism of nitrogen sources are low (ammonium repression). The gdhA10 lesion, which results in loss of nicotinamide adenine dinucleotide phosphate-linked glutamate dehydrogenase activity, has been shown to lead to partial relief of ammonium repression of three amidase enzymes as well as histidase. The areA102 lesion led to altered levels of these enzymes but did not greatly affect ammonium repression. The double mutant areA102,gdhA10 was almost completely insensitive to ammonium repression of two of the amidase enzymes and histidase. This suggests that an interaction between the areA and gdhA genes in determining responses to ammonium occurs. Growth of mycelium in medium containing l-glutamate has been found to result in lowered levels of all four enzymes, and this occurs in strains insensitive to ammonium repression. Very strong repression in all strains occurred during growth in medium containing l-glutamine. Relief of these repressive effects of glutamate and glutamine was blocked by cycloheximide. Glutamate and glutamine had similar effects on the production of extracellular protease activity, and growth on glutamine led to low levels of urate oxidase. In contrast to the above enzymes, nitrate reductase was insensitive to the effects of glutamine and glutamate, even though this enzyme is very sensitive to ammonium repression. Although other possibilities exist, it is suggested that there may be mechanisms of general control of nitrogen-catabolic enzymes other than ammonium repression.

摘要

在构巢曲霉于含铵培养基中生长期间,参与氮源分解代谢的大多数酶的比活性较低(铵阻遏)。gdhA10损伤导致烟酰胺腺嘌呤二核苷酸磷酸连接的谷氨酸脱氢酶活性丧失,已表明该损伤会导致三种酰胺酶以及组氨酸酶的铵阻遏得到部分缓解。areA102损伤导致这些酶的水平发生改变,但对铵阻遏影响不大。双突变体areA102,gdhA10对两种酰胺酶和组氨酸酶的铵阻遏几乎完全不敏感。这表明在确定对铵的反应时,areA和gdhA基因之间存在相互作用。已发现菌丝体在含L-谷氨酸的培养基中生长会导致所有四种酶的水平降低,并且在对铵阻遏不敏感的菌株中也会出现这种情况。在含L-谷氨酰胺的培养基中生长期间,所有菌株都出现了非常强烈的阻遏。环己酰亚胺阻断了谷氨酸和谷氨酰胺的这些阻遏作用。谷氨酸和谷氨酰胺对细胞外蛋白酶活性的产生具有相似的影响,并且在谷氨酰胺上生长会导致尿酸氧化酶水平较低。与上述酶不同,硝酸还原酶对谷氨酰胺和谷氨酸的作用不敏感,尽管该酶对铵阻遏非常敏感。尽管存在其他可能性,但有人认为可能存在除铵阻遏之外的氮分解代谢酶的一般控制机制。

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