FINE-STRUCTURE DELETION MAP AND COMPLEMENTATION ANALYSIS OF THE GLNA-GLNL-GLNG REGION IN ESCHERICHIA-COLI
FINE-STRUCTURE DELETION MAP AND COMPLEMENTATION ANALYSIS OF THE GLNA-GLNL-GLNG REGION IN ESCHERICHIA-COLI
复制标题
DOI：
10.1128/jb.150.3.1302-1313.1982
复制
发表时间：
1982-01-01
影响因子：
3.2
通讯作者：
TYLER, B
中科院分区：
文献类型：
--
作者：
MACNEIL, T;MACNEIL, D;TYLER, B
总共获得了399个独立的大肠杆菌突变体，它们在glnA区域具有点突变和插入突变。分离出的突变体包括 Gln- 和 Reg- 菌株（无法利用精氨酸作为氮源）。用 73 个含有 lambda 缺失的衍生物绘制突变图。 gln噬菌体。用λ进行互补分析。含有点突变的gln衍生物，赋予Gln-或Reg-表型。删除定位和互补分析将 24 个删除间隔中的 104 个突变分配给 glnA。 Reg-菌株中的突变被分配给2个基因：glnL和glnG。 glnL 在 12 个删除区间包含 131 个突变，glnG 在 10 个删除区间包含 164 个突变。基因顺序为glnA-glnL-glnG，从左到右转录。插入突变的极性表明glnL 和glnG 形成操纵子。 glnA 插入突变与 glnL 和 glnG 突变的互补分析显示大多数 glnL 和 glnG 等位基因上的 glnA 极性，表明 glnA 的转录可能进入 glnL-glnG 操纵子。 glnA 中分析的所有突变均赋予 Gln 表型。然而，化学诱变后分离出的 Gln- 菌株中超过一半含有 glnG 点突变。选择在氨存在下合成高水平谷氨酰胺合成酶（GlnC 表型）的突变体作为在glnD 中插入转座子Tn10 的菌株的回复体，并用染色体缺失进行定位。 15 个检查菌株中有 12 个的突变清楚地定位在 glnA 之外，可能在 glnL 中。
A total of 399 independent mutants of E. coli were obtained which have point and insertion mutations in the glnA region. Mutants isolated included Gln- and Reg- strains (unable to utilize arginine as an N source). Mutations were mapped with 73 deletion-containing derivatives of a .lambda. gln phage. Complementation analysis was performed with .lambda. gln derivatives containing point mutations which conferred a Gln- or Reg- phenotype. Deletion mapping and complementation analysis assigned 104 mutations in 24 deletion intervals to glnA. Mutations in Reg- strains were assigned to 2 genes, glnL and glnG. glnL contained 131 mutations in 12 deletion intervals and glnG contained 164 mutations in 10 deletion intervals. The gene order is glnA-glnL-glnG, transcribed from left to right. Polarity of insertion mutations indicates that glnL and glnG form an operon. Complementation analysis of glnA insertion mutations with glnL and glnG mutations showed polarity of glnA onto most glnL and glnG alleles, suggesting that transcription of glnA may proceed into the glnL-glnG operon. All mutations analyzed in glnA conferred a Gln- phenotype. However, over half of the Gln- strains isolated after chemical mutagenesis contained point mutations in glnG. Mutants which synthesized a high level of glutamine synthetase in the presence of ammonia (GlnC phenotype) were selected as revertants of a strain with a transposon Tn10 insertion in glnD and were mapped with chromosomal deletions. Mutations in 12 of 15 examined strains clearly map outside of glnA, probably in glnL.