基因astE调控微生物抵御丁醇胁迫的生理机制解析

发布时间：2018-06-09 06:18

本文选题：astE基因 + 大肠杆菌　；参考：《基因组学与应用生物学》2017年01期

【摘要】：探究敲除精氨酸代谢途径关键酶ast E对大肠杆菌抵御丁醇胁迫能力的影响。借助氨基酸分析仪全面分析ast E基因敲除对细胞内外游离氨基酸水平的变化。同时,通过测定ast E缺失突变株抵御丁醇和酸胁迫的能力,并分析两者之间的联系。研究表明:与对照菌株BW25113相比,突变株△ast E抵御丁醇胁迫和酸胁迫的能力显著提高,分别提高了30%(8 g/L丁醇)和54.5%(p H 3.0)。同时,通过胞内外氨基酸分析发现,高浓度丁醇胁迫可抑制BW25113和△ast E合成谷氨酸的能力,使其浓度分别降低73.6%和89.1%。在此基础上,外源添加精氨酸实验表明:适量精氨酸能有效提高细胞抵御高浓度丁醇胁迫的能力。敲除精氨酸代谢途径关键酶ast E可显著提高大肠杆菌抵御丁醇胁迫的能力,且其调控机制与耐酸胁迫密切相关。
[Abstract]:To explore the effect of knockout arginine metabolic pathway key enzyme ast E on the ability of Escherichia coli to resist butanol stress. The changes of free amino acids in ast E gene knockout cells were analyzed by amino acid analyzer. At the same time, the ability of ast E deletion mutant to resist butanol and acid stress was determined and the relationship between them was analyzed. The results showed that compared with the control strain BW25113, the ability of the mutant ast E to resist butanol stress and acid stress was significantly increased by 30g / L butanol and 54.5g / L butanol, respectively. At the same time, it was found that high concentration of butanol could inhibit the ability of BW25113 and ast E to synthesize glutamate by 73.6% and 89.1%, respectively. On this basis, the experiment of exogenous arginine showed that arginine could effectively improve the ability of cells to resist high concentration of butanol stress. Knockout of the key enzyme of arginine metabolism pathway ast E can significantly improve the ability of Escherichia coli to resist butanol stress, and its regulatory mechanism is closely related to acid stress.
【作者单位】：广西科学院非粮生物质酶解国家重点实验室国家非粮生物质能源工程技术研究中心广西生物炼制重点实验室;
【基金】：国家自然科学基金项目(21366007) 广西自然科学基金项目(2015GXNSFBA139048,2015GXNSFBA13-9084cb-p C,2014GXNSFBA118129,2014GXNSFAA118078) 广西科技攻关项目桂科重(1598004-3,14122004-5) 广西科学院基本科研业务费(15YJ22SW05,13YJ22SW02)共同资助
【分类号】：Q93

【相似文献】