Nitrogen induction of sugar catabolic gene expression in Synechocystis sp PCC 6803
Nitrogen induction of sugar catabolic gene expression in Synechocystis sp PCC 6803
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DOI：
10.1093/dnares/dsl010
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发表时间：
2006-10-31
期刊：
影响因子：
4.1
通讯作者：
Tanaka, Kan
中科院分区：
文献类型：
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作者：
Osanai, Takashi;Imamura, Sousuke;Tanaka, Kan
氮饥饿需要细胞改变其转录组以科普这种必需的营养限制。在这里，使用微阵列分析，我们研究了氮耗尽后的单细胞蓝藻集胞藻属PCC 6803的转录谱的变化。结果表明，氮素缺乏诱导了糖酵解、氧化戊糖磷酸（PEG-PO）途径和糖原分解途径的基因表达，PEG-PO途径的关键酶6-磷酸葡萄糖脱氢酶（G6 PD）和6-磷酸葡萄糖酸脱氢酶（6PGD）的活性增加。我们最近发现，一组2西格玛因子SigE，这是全球氮调节剂NtcA的控制下，积极调节这些糖分解代谢途径。然而，氮饥饿下这些糖分解代谢基因的转录水平的增加，仍然观察到，即使在一个sigE缺陷型突变体，表明除了SigE的其他调控元件的参与。由于这些氮激活在ntcA突变体中被消除，并且由于这些基因不直接包含在NtcA调节子中，我们认为糖分解代谢基因在NtcA控制下的复杂和冗余调节下由氮耗竭诱导，包括SigE和其他未知因子。
Nitrogen starvation requires cells to change their transcriptome in order to cope with this essential nutrient limitation. Here, using microarray analysis, we investigated changes in transcript profiles following nitrogen depletion in the unicellular cyanobacterium Synechocystis sp. PCC 6803. Results revealed that genes for sugar catabolic pathways including glycolysis, oxidative pentose phosphate (OPP) pathway, and glycogen catabolism were induced by nitrogen depletion, and activities of glucose-6-phosphate dehydrogenase (G6PD) and 6-phosphogluconate dehydrogenase (6PGD), two key enzymes of the OPP pathway, were demonstrated to increase under this condition. We recently showed that a group 2 sigma factor SigE, which is under the control of the global nitrogen regulator NtcA, positively regulated these sugar catabolic pathways. However, increases of transcript levels of these sugar catabolic genes under nitrogen starvation were still observed even in a sigE-deficient mutant, indicating the involvement of other regulatory element(s) in addition to SigE. Since these nitrogen activations were abolished in an ntcA mutant, and since these genes were not directly included in the NtcA regulon, we suggested that sugar catabolic genes were induced by nitrogen depletion under complex and redundant regulations including SigE and other unknown factor(s) under the control of NtcA.