ModE-dependent molybdate regulation of the molybdenum cofactor operon moa in Escherichia coli
ModE-dependent molybdate regulation of the molybdenum cofactor operon moa in Escherichia coli
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DOI：
10.1128/jb.182.24.7035-7043.2000
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发表时间：
2000-12-01
影响因子：
3.2
通讯作者：
Boxer, DH
中科院分区：
文献类型：
--
作者：
Anderson, LA;McNairn, E;Boxer, DH
在厌氧条件下，MOA基因座的表达得到增强，但当细菌能够合成活性钼辅因子时，MOA基因座的表达受到抑制，MOA基因座编码的酶是多蝶呤生物合成所需的。此外，moa的表达表现出强烈的表达要求。MOA转录的抑制增强完全依赖于腺苷酸结合蛋白ModE，其也介导编码高亲和力腺苷酸摄取系统的mod操纵子的抑制。由于钼辅因子充足的菌株中MOA的阻遏，MOA的正向调节仅在不能产生活性辅因子的菌株中显示。moa的转录由moaA基因上游的两个sigma-70型启动子控制。覆盖moaA上游区域的缺失突变允许单独研究每个启动子。远端启动子是Fnr依赖的厌氧增强的位点。moa的启动子诱导作用发生在近端启动子。钼酸盐-ModE与该启动子的-35区域相邻结合，作为moa的直接正调节剂。钼辅因子的抑制似乎也在近端转录起始位点发挥作用，但其机制仍有待确定。生长培养基中的钨酸盐以两种方式影响moa的表达。首先，它可以作为ModE介导的调节的功能性β-内酰胺类似物。其次，钨酸盐导致钼辅因子对moa的抑制作用丧失，提出已知在这种条件下形成的钼辅因子的钨衍生物在导致moa的抑制作用方面是无效的。MOA的复杂的控制进行了讨论，在有关的细菌中的辅酶的合成。
The expression of the moa locus, which encodes enzymes required for molybdopterin biosynthesis, is enhanced under anaerobiosis but repressed when the bacterium is able to synthesize active molybdenum cofactor. In addition, moa expression exhibits a strong requirement for molybdate. The molybdate enhancement of moa transcription is fully dependent upon the molybdate-binding protein, ModE, which also mediates molybdate repression of the mod operon encoding the high-affinity molybdate uptake system. Due to the repression of moa in molybdenum cofactor-sufficient strains, the positive molybdate regulation of moa is revealed only in strains unable to make the active cofactor. Transcription of moa is controlled at two sigma-70-type promoters immediately upstream of the moaA gene. Deletion mutations covering the region upstream of moaA have allowed each of the promoters to be studied in isolation. The distal promoter is the site of the anaerobic enhancement which is Fnr-dependent. The molybdate induction of moa is exerted at the proximal promoter. Molybdate-ModE binds adjacent to the -35 region of this promoter, acting as a direct positive regulator of moa. The molybdenum cofactor repression also appears to act at the proximal transcriptional start site, but the mechanism remains to be established. Tungstate in the growth medium affects moa expression in two ways. Firstly, it can act as a functional molybdate analogue for the ModE-mediated regulation. Secondly, tungstate brings about the loss of the molybdenum cofactor repression of moa, It is proposed that the tungsten derivative of the molybdenum cofactor, which is known to be formed under such conditions, is ineffective in bringing about repression of moa. The complex control of moa is discussed in relation to the synthesis of molybdoenzymes in the bacterium.