Stanbrough M, Rowen D W, Magasanik B
Department of Biology, Massachusetts Institute of Technology, Cambridge 02139, USA.
Proc Natl Acad Sci U S A. 1995 Oct 10;92(21):9450-4. doi: 10.1073/pnas.92.21.9450.
We have isolated the NIL1 gene, whose product is an activator of the transcription of nitrogen-regulated genes, by virtue of the homology of its zinc-finger domain to that of the previously identified activator, the product of GLN3. Disruption of the chromosomal NIL1 gene enabled us to compare the effects of Gln3p and of Nil1p on the expression of the nitrogen-regulated genes GLN1, GDH2, and GAP1, coding respectively for glutamine synthetase, NAD-linked glutamate dehydrogenase, and general amino acid permease. Our results show that the nature of GATAAG sequence that serve as the upstream activation sequence elements for these genes determines their abilities to respond to Gln3p and Nil1p. The results further indicate that Gln3p is inactivated by an increase in the intracellular concentration of glutamine and that Nil1p is inactivated by an increase in intracellular glutamate.
我们通过其锌指结构域与先前鉴定的激活因子GLN3的产物的同源性，分离出了NIL1基因，该基因的产物是氮调节基因转录的激活因子。染色体NIL1基因的破坏使我们能够比较Gln3p和Nil1p对氮调节基因GLN1、GDH2和GAP1表达的影响，这三个基因分别编码谷氨酰胺合成酶、NAD连接的谷氨酸脱氢酶和通用氨基酸通透酶。我们的结果表明，作为这些基因上游激活序列元件的GATAAG序列的性质决定了它们对Gln3p和Nil1p作出反应的能力。结果还进一步表明，谷氨酰胺细胞内浓度的增加会使Gln3p失活，而细胞内谷氨酸浓度的增加会使Nil1p失活。
