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Deeper below the surface—transcriptional changes in selected genes of Clostridium beijerinckii in response to butanol shock
MicrobiologyOpen ( IF 3.9 ) Pub Date : 2020-12-14 , DOI: 10.1002/mbo3.1146
Petra Patakova 1 , Jan Kolek 1 , Katerina Jureckova 2 , Barbora Branska 1 , Karel Sedlar 2 , Maryna Vasylkivska 1 , Ivo Provaznik 2
Affiliation  

The main bottleneck in the return of industrial butanol production from renewable feedstock through acetone–butanol–ethanol (ABE) fermentation by clostridia, such as Clostridium beijerinckii, is the low final butanol concentration. The problem is caused by the high toxicity of butanol to the production cells, and therefore, understanding the mechanisms by which clostridia react to butanol shock is of key importance. Detailed analyses of transcriptome data that were obtained after butanol shock and their comparison with data from standard ABE fermentation have resulted in new findings, while confirmed expected population responses. Although butanol shock resulted in upregulation of heat shock protein genes, their regulation is different than was assumed based on standard ABE fermentation transcriptome data. While glucose uptake, glycolysis, and acidogenesis genes were downregulated after butanol shock, solventogenesis genes were upregulated. Cyclopropanation of fatty acids and formation of plasmalogens seem to be significant processes involved in cell membrane stabilization in the presence of butanol. Surprisingly, one of the three identified Agr quorum‐sensing system genes was upregulated. Upregulation of several putative butanol efflux pumps was described after butanol addition and a large putative polyketide gene cluster was found, the transcription of which seemed to depend on the concentration of butanol.

中文翻译:

表面以下更深的地方——拜氏梭菌响应丁醇休克的选定基因的转录变化

通过梭状芽胞杆菌(例如拜氏梭菌)发酵丙酮-丁醇-乙醇 (ABE) 从可再生原料中恢复工业丁醇生产的主要瓶颈, 是低的最终丁醇浓度。该问题是由丁醇对生产细胞的高毒性引起的,因此了解梭状芽胞杆菌对丁醇休克反应的机制至关重要。对丁醇休克后获得的转录组数据的详细分析以及它们与标准 ABE 发酵数据的比较产生了新的发现,同时证实了预期的群体反应。尽管丁醇休克导致热休克蛋白基因的上调,但它们的调节与基于标准 ABE 发酵转录组数据的假设不同。虽然葡萄糖摄取、糖酵解和酸生成基因在丁醇休克后下调,但溶剂生成基因上调。脂肪酸的环丙烷化和缩醛磷脂的形成似乎是在丁醇存在下参与细胞膜稳定的重要过程。令人惊讶的是,三个确定的 Agr 群体感应系统基因之一被上调。在添加丁醇后描述了几个推定的丁醇外排泵的上调,并发现了一个大的推定聚酮化合物基因簇,其转录似乎取决于丁醇的浓度。
更新日期:2021-02-16
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