Coffman J A, el Berry H M, Cooper T G
Department of Microbiology and Immunology, University of Tennessee, Memphis 38163.
J Bacteriol. 1994 Dec;176(24):7476-83. doi: 10.1128/jb.176.24.7476-7483.1994.
Many of the gene products that participate in nitrogen metabolism are sensitive to nitrogen catabolite repression (NCR), i.e., their expression is decreased to low levels when readily used nitrogen sources such as asparagine are provided. Previous work has shown this NCR sensitivity requires the cis-acting UASNTR element and trans-acting GLN3. Here, we extend the analysis to include the response of their expression to deletion of the URE2 locus. The expression of these nitrogen catabolic genes becomes, to various degrees, NCR insensitive in the ure2 deletion. This response is shown to be mediated through the GATAA-containing UASNTR element and supports the current idea that the NCR regulatory circuit involves the following steps: environmental signal-->URE2-->GLN3-->UASNTR operation-->NCR-sensitive gene expression. The various responses of the nitrogen catabolic genes' expression to deletion of the URE2 locus also indicate that not all NCR is mediated through URE2.
许多参与氮代谢的基因产物对氮分解代谢物阻遏(NCR)敏感,即当提供容易利用的氮源(如天冬酰胺)时,它们的表达会降至低水平。先前的研究表明,这种NCR敏感性需要顺式作用的UASNTR元件和反式作用的GLN3。在这里,我们将分析扩展到包括它们的表达对URE2基因座缺失的反应。在ure2缺失的情况下,这些氮分解代谢基因的表达在不同程度上变得对NCR不敏感。这种反应被证明是通过含GATAA的UASNTR元件介导的,并支持了目前关于NCR调节回路涉及以下步骤的观点:环境信号→URE2→GLN3→UASNTR作用→NCR敏感基因表达。氮分解代谢基因表达对URE2基因座缺失的各种反应也表明,并非所有的NCR都是通过URE2介导的。