Jacobsen E, Schaart J G, Warner R L
Biochem Genet. 1987 Feb;25(1-2):143-51. doi: 10.1007/BF00498957.
Two nitrate reductase (NaR)-deficient mutants of pea (Pisum sativum L.), E1 and A300, both disturbed in the molybdenum cofactor function and isolated, respectively, from cv Rondo and cv Juneau, were tested for allelism and were compared in biochemical and growth characteristics. The F1 plants of the cross E1 X A300 possessed NaR and xanthine dehydrogenase (XDH) activities comparable to those of the wild types, indicating that these mutants belong to different complementation groups, representing two different loci. Therefore, mutant E1 represents, besides mutant A300 and the allelic mutants A317 and A334, a third locus governing NaR and is assigned the gene destignation nar 3. In comparison with the wild types, cytochrome c reductase activity was increased in both mutants. The mutants had different cytochrome c reductase distribution patterns, indicating that mutant A300 could be disturbed in the ability to dimerize NaR apoprotein monomers, and mutant E1 in the catalytic function of the molybdenum cofactor. In growth characteristics studied, A300 did not differ from the wild types, whereas fully grown leaves of mutant E1 became necrotic in soil and in liquid media containing nitrate.
从豌豆（Pisum sativum L.）品种Rondo和Juneau中分别分离出的两个硝酸盐还原酶（NaR）缺陷型突变体E1和A300，二者钼辅因子功能均受到干扰。对它们进行了等位性测试，并比较了生化和生长特性。杂交组合E1×A300的F1植株具有与野生型相当的NaR和黄嘌呤脱氢酶（XDH）活性，这表明这些突变体属于不同的互补群，代表两个不同的基因座。因此，除了突变体A300以及等位突变体A317和A334之外，突变体E1代表了控制NaR的第三个基因座，并被赋予基因命名nar 3。与野生型相比，两个突变体中的细胞色素c还原酶活性均有所增加。突变体具有不同的细胞色素c还原酶分布模式，这表明突变体A300可能在NaR脱辅基蛋白单体二聚化能力方面受到干扰，而突变体E1则在钼辅因子的催化功能方面受到干扰。在所研究的生长特性方面，A300与野生型没有差异，而突变体E1完全展开的叶片在含有硝酸盐的土壤和液体培养基中会坏死。
