Nitrogen regulatory protein C-controlled genes of Escherichia coli:: Scavenging as a defense against nitrogen limitation
Nitrogen regulatory protein C-controlled genes of Escherichia coli:: Scavenging as a defense against nitrogen limitation
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DOI：
10.1073/pnas.97.26.14674
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发表时间：
2000-12-19
影响因子：
11.1
通讯作者：
Kustu, S
中科院分区：
文献类型：
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作者：
Zimmer, DP;Soupene, E;Kustu, S
肠道细菌的氮调节蛋白 C (NtrC) 激活基因/操纵子的转录，其产物最大限度地减少氮限制条件下生长的减慢。揭示氮限制条件下生长减慢。为了揭示大肠杆菌的 NtrC 调节子，我们使用 DNA 微阵列将过表达 NtrC 激活基因 [glnL(Up)] 的突变菌株中的 mRNA 水平与具有 ntrC (glnG) 无效等位基因的菌株中的 mRNA 水平进行了比较。两种菌株都可以在氮过量的条件下生长。因此，我们可以避免因生长缓慢或氮限制本身引起的基因表达差异。按基因组顺序重新排列微阵列中的点图像使我们能够检测所有已知受 NtrC 控制的操纵子，并有助于检测许多新操纵子。许多操纵子编码含氮化合物的运输系统，包括细胞壁合成过程中回收的化合物，因此清除似乎是对氮限制的主要反应。总之，大约 2% 的大肠杆菌基因组似乎处于 NtrC 控制之下，尽管某些操纵子的转录依赖于氮同化控制蛋白，该蛋白充当 NtrC 和 sigma (70) 依赖性启动子之间的衔接子。
Nitrogen regulatory protein C (NtrC) of enteric bacteria activates transcription of genes/operons whose products minimize the slowing of growth under nitrogen-limiting conditions. To reveal slowing of growth under nitrogen-limiting conditions. To reveal the NtrC regulon of Escherichia coli we compared mRNA levels in a mutant strain that overexpresses NtrC-activated genes [glnL(Up)] to those in a strain with an ntrC (glnG) null allele by using DNA microarrays. Both strains could be grown under conditions of nitrogen excess. Thus, we could avoid differences in gene expression caused by slow growth or nitrogen limitation per se. Rearranging the spot images from microarrays in genome order allowed us to detect all of the operons known to be under NtrC control and facilitated detection of a number of new ones. Many of these operons encode transport systems for nitrogen-containing compounds, including compounds recycled during cell-wall synthesis, and hence scavenging appears to be a primary response to nitrogen limitation. In all, approximate to2% of the E. coli genome appears to be under NtrC control, although transcription of some operons depends on the nitrogen assimilation control protein, which serves as an adapter between NtrC and sigma (70)-dependent promoters.