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首页> 外文期刊>Journal of bacteriology >Regulation of the aromatic pathway in the cyanobacterium Synechococcus sp. strain Pcc6301 (Anacystis nidulans).
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Regulation of the aromatic pathway in the cyanobacterium Synechococcus sp. strain Pcc6301 (Anacystis nidulans).

机译:蓝藻Synechococcus sp。中芳香途径的调控。菌株Pcc6301(Anacystis nidulans)。

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摘要

A pattern of allosteric control for aromatic biosynthesis in cyanobacteria relies upon early-pathway regulation as the major control point for the entire branched pathway. In Synechococcus sp. strain PCC6301 (Anacystis nidulans), two enzymes which form precursors for L-phenylalanine biosynthesis are subject to control by feedback inhibition. 3-Deoxy-D-arabino-heptulosonate 7-phosphate synthase (first pathway enzyme) is feedback inhibited by L-tyrosine, whereas prephenate dehydratase (enzyme step 9) is feedback inhibited by L-phenylalanine and allosterically activated by L-tyrosine. Mutants lacking feedback inhibition of prephenate dehydratase excreted relatively modest quantities of L-phenylalanine. In contrast, mutants deregulated in allosteric control of 3-deoxy-D-arabino-heptulosonate 7-phosphate synthase excreted large quantities of L-phenylalanine (in addition to even greater quantities of L-tyrosine). Clearly, in the latter mutants, the elevated levels of prephenate must overwhelm the inhibition of prephenate dehydratase by L-phenylalanine, an effect assisted by increased intracellular L-tyrosine, an allosteric activator. The results show that early-pathway flow regulated in vivo by 3-deoxy-D-arabino-heptulosonate 7-phosphate synthase is the dominating influence upon metabolite flow-through to L-phenylalanine. L-Tyrosine biosynthesis exemplifies such early-pathway control even more simply, since 3-deoxy-D-arabino-heptulosonate 7-phosphate synthase is the sole regulatory enzyme subject to end-product control by L-tyrosine.
机译:蓝藻中芳香族生物合成的变构控制模式依赖于早期途径调节,是整个分支途径的主要控制点。在Synechococcus sp。菌株PCC6301(Anacystis nidulans),形成L-苯丙氨酸生物合成前体的两种酶通过反馈抑制来控制。 L-酪氨酸可抑制3-脱氧-D-阿拉伯糖庚酸七磷酸合酶(第一途径酶),而L-苯丙氨酸可抑制苯甲酸酯脱水酶(酶步骤9)并由L-酪氨酸变构激活。缺乏对苯甲酸酯脱水酶的反馈抑制作用的突变体会排出相对少量的L-苯丙氨酸。相反,在3-脱氧-D-阿拉伯糖-庚酸七磷酸合酶的变构控制中失控的突变体会分泌大量的L-苯丙氨酸(此外还会分泌更多的L-酪氨酸)。显然,在后一种突变体中,高水平的苯甲酸酯必须克服L-苯丙氨酸对苯甲酸酯脱水酶的抑制作用,而这种作用是通过变构激活剂细胞内L-酪氨酸增加而实现的。结果表明,体内3-脱氧-D-阿拉伯-庚酸七磷酸合酶调节的早期途径流动是代谢物流向L-苯丙氨酸的主要影响。 L-酪氨酸的生物合成甚至更简单地举例说明了这种早期途径的控制,因为3-脱氧-D-阿拉伯糖-庚酸七磷酸合酶是唯一受L-酪氨酸控制的终产物调节酶。

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