Abstract:

To explore the effect of ethanol synthesize in Synechocystis sp. PCC 6803， the exogenous ethanol-producing genes were introduced and the competitive metabolic pathway of pyruvate to lactate was deleted. The pyruvate decarboxylase gene （pdc） from Synechocystis sp. PCC 6803 and the NADPH-dependent aldehyde reductase gene （yqhD） from Escherichia coli in this study were introduced and combined for expression under the drove of the light intensity promoter PrbcL to synthesize ethanol in Synechocystis sp. PCC 6803. Based of this， the slr1556 gene encoding lactate dehydrogenase in Synechocystis sp. PCC6803 was further knocked out to increase the content of pyruvate， the precursor for ethanol synthesis and promote the ethanol production. The results showed that by knocking out the slr1556 gene， the content of pyruvate was improved and the synthesized ethanol output was significantly increased. The block of the competitive metabolic pathway of the conversion of pyruvate to lactic acid can effectively promote the accumulation of pyruvate and then promote the production of ethanol.

Key words: ethanol, lactate, Synechocystis sp. PCC 6803, precursor, pyruvate

摘要：

探究在集胞藻PCC 6803中引入外源乙醇合成基因并敲除集胞藻PCC 6803中编码乳酸脱氢酶的slr1556基因对生物合成乙醇的影响。在集胞藻PCC 6803中引入来源于运动型发酵单胞菌的丙酮酸脱羧酶基因（pdc）与大肠杆菌的NADPH依赖型醛还原酶基因（yqhD）光强启动子PrbcL的驱动下组合表达，生物合成乙醇。在此基础上进一步敲除集胞藻PCC 6803中编码乳酸脱氢酶的slr1556基因，以提高乙醇合成前体丙酮酸含量，促进乙醇的生产。结果显示敲除slr1556基因可以提高丙酮酸含量并显著增加乙醇的产量。竞争性丙酮酸转化乳酸代谢途径的阻断可以有效促进丙酮酸的累积，进而促进乙醇的生产。

关键词: 乙醇, 乳酸, 集胞藻PCC 6803, 前体, 丙酮酸