PHYSIOLOGICAL AND GENETIC-ANALYSIS OF THE CARBON REGULATION OF THE NAD-DEPENDENT GLUTAMATE-DEHYDROGENASE OF SACCHAROMYCES-CEREVISIAE
PHYSIOLOGICAL AND GENETIC-ANALYSIS OF THE CARBON REGULATION OF THE NAD-DEPENDENT GLUTAMATE-DEHYDROGENASE OF SACCHAROMYCES-CEREVISIAE
复制标题
DOI：
10.1128/mcb.11.9.4455
复制
发表时间：
1991-09-01
影响因子：
5.3
通讯作者：
MAGASANIK, B
中科院分区：
文献类型：
--
作者：
COSCHIGANO, PW;MILLER, SM;MAGASANIK, B
我们发现，酿酒酵母细胞有一个NAD依赖性谷氨酸脱氢酶（NAD-GDH;由GDH 2基因编码）的水平升高时，生长与一个nonfermentable碳源或葡萄糖的限制量，即使在抑制氮源谷氨酰胺的存在下。 发现这种调节是转录的，并且鉴定了足以在呼吸生长条件下激活转录的上游激活位点（GDH 2 UAS（c））。 发现该UAS与该基因的氮源调节所必需的相邻元件是可分离的，并且在用活化氮源谷氨酸盐生长期间表达NAD-GDH所需的GLN 3基因产物缺陷的菌株在用活化碳源生长期间不受NAD-GDH表达的影响。 发现并表征了两类突变，其阻止NAD-GDH响应于不可发酵碳源的生长而正常激活，但不影响NAD-GDH的氮调节表达。 碳调节GDH 2被发现是正常的hxk 2，hap 3和hap 4菌株，并在ssn 6菌株中仅略有改变，因此，在与以前确定的葡萄糖抑制基因的调节相比，一个新的途径似乎参与GDH 2的调节。
We found that cells of Saccharomyces cerevisiae have an elevated level of the NAD-dependent glutamate dehydrogenase (NAD-GDH; encoded by the GDH2 gene) when grown with a nonfermentable carbon source or with limiting amounts of glucose, even in the presence of the repressing nitrogen source glutamine. This regulation was found to be transcriptional, and an upstream activation site (GDH2 UAS(c)) sufficient for activation of transcription during respiratory growth conditions was identified. This UAS was found to be separable from a neighboring element which is necessary for the nitrogen source regulation of the gene, and strains deficient for the GLN3 gene product, required for expression of NAD-GDH during growth with the activating nitrogen source glutamate, were unaffected for the expression of NAD-GDH during growth with activating carbon sources. Two classes of mutations which prevented the normal activation of NAD-GDH in response to growth with nonfermentable carbon sources, but which did not affect the nitrogen-regulated expression of NAD-GDH, were found and characterized. Carbon regulation of GDH2 was found to be normal in hxk2, hap3, and hap4 strains and to be only slightly altered in a ssn6 strain; thus, in comparison with the regulation of previously identified glucose-repressed genes, a new pathway appears to be involved in the regulation of GDH2.