Dantzig A H, Zurowski W K, Ball T M, Nason A
J Bacteriol. 1978 Feb;133(2):671-9. doi: 10.1128/jb.133.2.671-679.1978.
Synthesis of wild-type Neurospora crassa assimilatory nitrate reductase is induced in the presence of nitrate ions and repressed in the presence of ammonium ions. Effects of several Neurospora mutations on the regulation of this enzyme are shown: (i) the mutants, nit-1 and nit-3, involving separate lesions, lack reduced nicotinamide adenine dinucleotide (NADPH)-nitrate reductase activity and at least one of three other activities associated with the wild-type enzyme. The two mutants do not require the presence of nitrate for induction of their aberrant nitrate reductases and are constitutive for their component nitrate reductase activities in the absence of ammonium ions. (ii) An analog of the wild-type enzyme (similar to the nit-1 enzyme) is formed when wild type is grown in a medium in which molybdenum has been replaced by vanadium or tungsten; the resulting enzyme lacks NADPH-nitrate reductase activity. Unlike nit-1, wild type produced this analog only in the presence of nitrate. Contaminating nitrate does not appear to be responsible for the observed mutants' activities. Nitrate reductase is proposed to be autoregulated. (iii) Mutants (am) lacking NADPH-dependent glutamate dehydrogenase activity partially escape ammonium repression of nitrate reductase. The presence of nitrate is required for the enzyme's induction. (iv) A double mutant, nit-1 am-2, proved to be an ideal test system to study the repressive effects of nitrogen-containing metabolites on the induction of nitrate reductase activity. The double mutant does not require nitrate for induction of nitrate reductase, and synthesis of the enzyme is not repressed by the presence of high concentrations of ammonium ions. It is, however, repressed by the presence of any one of six amino acids. Nitrogen metabolites (other than ammonium) appear to be responsible for the mediation of "ammonium repression."
野生型粗糙脉孢菌同化型硝酸还原酶的合成在硝酸根离子存在时被诱导，而在铵离子存在时被抑制。展示了几种脉孢菌突变对该酶调控的影响：(i) 涉及不同损伤的突变体nit-1和nit-3缺乏还原型烟酰胺腺嘌呤二核苷酸（NADPH）-硝酸还原酶活性以及与野生型酶相关的其他三种活性中的至少一种。这两个突变体在诱导其异常硝酸还原酶时不需要硝酸根离子的存在，并且在没有铵离子的情况下其组成型硝酸还原酶活性是组成型的。(ii) 当野生型在钼被钒或钨取代的培养基中生长时，会形成一种野生型酶的类似物（类似于nit-1酶）；产生的酶缺乏NADPH-硝酸还原酶活性。与nit-1不同，野生型仅在硝酸根离子存在时产生这种类似物。污染的硝酸根似乎与观察到的突变体活性无关。硝酸还原酶被认为是自我调节的。(iii) 缺乏NADPH依赖性谷氨酸脱氢酶活性的突变体（am）部分逃避了铵对硝酸还原酶的抑制。该酶的诱导需要硝酸根离子的存在。(iv) 双突变体nit-1 am-2被证明是研究含氮代谢物对硝酸还原酶活性诱导的抑制作用的理想测试系统。双突变体在诱导硝酸还原酶时不需要硝酸根离子，并且该酶的合成不会被高浓度铵离子的存在所抑制。然而，它会被六种氨基酸中的任何一种的存在所抑制。氮代谢物（除铵外）似乎是“铵抑制”介导的原因。
