Transcriptional organization and regulation of the L-idonic acid pathway (GntII system) in Escherichia coli
Transcriptional organization and regulation of the L-idonic acid pathway (GntII system) in Escherichia coli
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DOI：
10.1128/jb.186.5.1388-1397.2004
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发表时间：
2004-03-01
影响因子：
3.2
通讯作者：
Conway, T
中科院分区：
文献类型：
--
作者：
Bausch, C;Ramsey, M;Conway, T
编码L-艾多酸分解代谢途径的idn基因的遗传组织被表征。单顺反子 idnK 基因的转录方式与 idnDOTR 基因不同，后者被证明可形成操纵子。 idnK 和 idnD 基因之间的 215 bp 调控区包含方向相反的启动子，其转录起始位点映射到相对于起始密码子的位置 -26 和 -29。调控区还包含一个位于两个启动子之间的推定 IdnR/GntR 结合位点、idnD 上游的 CRP 结合位点和 idnK 上游的 UP 元件。 L-Adonate 途径的基因显示受到分解代谢物抑制的控制。对无法使 L-艾酮酸和 5-酮葡萄糖酸相互转化的非极性 idnD 突变体中的 idnD- 和 idnK-lacZ 融合体进行的分析表明，任一化合物都可以诱导该途径。 L-艾杜酸途径首先被定性为 D-葡萄糖酸分解代谢 (GntII) 的辅助途径，该途径是由 GntI（初级葡萄糖酸系统）突变体中的 D-葡萄糖酸诱导的。在这里，我们表明 idnK 和 idnD 操纵子是由 GntI 系统突变体中的 D-葡萄糖酸诱导的，可能是通过从 D-葡萄糖酸内源形成 5-酮葡萄糖酸来诱导的。因此，GntII 系统的调节适合该途径，该途径主要参与 L-艾多酸分解代谢；在阻断 GntI 系统的条件下，D-葡萄糖酸可以诱导 GntII 系统。
The genetic organization of the idn genes that encode the pathway for L-idonate catabolism was characterized. The monocistronic idnK gene is transcribed divergently from the idnDOTR genes, which were shown to form an operon. The 215-bp regulatory region between the idnK and idnD genes contains promoters in opposite orientation with transcription start sites that mapped to positions -26 and -29 with respect to the start codons. The regulatory region also contains a single putative IdnR/GntR binding site centered between the two promoters, a CRP binding site upstream of idnD, and an UP element upstream of idnK. The genes of the L-Adonate pathway were shown to be under catabolite repression control. Analysis of idnD- and idnK-lacZ fusions in a nonpolar idnD mutant that is unable to interconvert L-idonate and 5-ketogluconate indicated that either compound could induce the pathway. The L-idonate pathway was first characterized as a subsidiary pathway for D-gluconate catabolism (GntII), which is induced by D-gluconate in a GntI (primary gluconate system) mutant. Here we showed that the idnK and idnD operons are induced by D-gluconate in a GntI system mutant, presumably by endogenous formation of 5-ketogluconate from D-gluconate. Thus, the regulation of the GntII system is appropriate for this pathway, which is primarily involved in L-idonate catabolism; the GntII system can be induced by D-gluconate under conditions that block the GntI system.