Honglun Yuan1, Yong Xu2, Yaozhong Chen2, Yangyang Zhan2, Xuetuan Wei3, Lu Li3, Dong Wang2, Penghui He2, Shengqing Li4, Shouwen Chen5,6. 1. State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, No. 1 Shizishan Street, Hongshan District, Wuhan, 430070, Hubei, China. 2. State Key Laboratory of Biocatalysis and Enzyme Engineering, Environmental Microbial Technology Center of Hubei Province, College of Life Sciences, Hubei University, Wuhan, 430062, China. 3. College of Food Science and Technology, Huazhong Agricultural University, Wuhan, 430070, China. 4. College of Sciences, Huazhong Agricultural University, Wuhan, 430070, China. 5. State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, No. 1 Shizishan Street, Hongshan District, Wuhan, 430070, Hubei, China. MEL212@126.com. 6. State Key Laboratory of Biocatalysis and Enzyme Engineering, Environmental Microbial Technology Center of Hubei Province, College of Life Sciences, Hubei University, Wuhan, 430062, China. MEL212@126.com.
Abstract
INTRODUCTION: Acetoin serves as a high value-added platform with a broad range of applications, and can be effectively produced by Bacillus licheniformis. However, its toxicity to the producing strain hinders the higher acetoin production, and current knowledge about the acetoin resistance mechanisms of B. licheniformis is quite limited. OBJECTIVES: To comprehensively investigate the metabolic changes in B. licheniformis under acetoin stress. METHODS: We used gas chromatography-mass spectrometry based untargeted metabolomics approach to measure the metabolic profiles of B. licheniformis under 20, 40 and 80 g/L acetoin stress. Transcriptional analysis was conducted to verify the metabolomics results. RESULTS: A total of 119 metabolites were identified in our experiment. The metabolic responses of B. licheniformis to acetoin stress were as follows: (i) pentose phosphate pathway and tricarboxylic acid (TCA) cycle were negatively affected by acetoin stress. In turn, glyoxylate cycle was activated to supply malic acid. (ii) Acetoin stress induced the accumulation of serine, valine, leucine and protective osmolytes (glycine and proline). (iii) Acetoin stress induced a higher saturated fatty acid ratio, which indicated a lower fluidity of cell membrane that could inhibit the entry of acetoin into cytoplasm. (iv) Synthesis of phosphatidylserine was enhanced, and phosphatidylethanolamine content was probably increased under acetoin stress. CONCLUSIONS: This study revealed the metabolic perturbations of B. licheniformis to acetoin stress. In response to acetoin stress, glyoxylate cycle was activated, protective osmolytes were accumulated, saturated fatty acid ratio was elevated and synthesis of phosphatidylserine was enhanced in B. licheniformis.
INTRODUCTION:Acetoin serves as a high value-added platform with a broad range of applications, and can be effectively produced by Bacillus licheniformis. However, its toxicity to the producing strain hinders the higher acetoin production, and current knowledge about the acetoin resistance mechanisms of B. licheniformis is quite limited. OBJECTIVES: To comprehensively investigate the metabolic changes in B. licheniformis under acetoin stress. METHODS: We used gas chromatography-mass spectrometry based untargeted metabolomics approach to measure the metabolic profiles of B. licheniformis under 20, 40 and 80 g/L acetoin stress. Transcriptional analysis was conducted to verify the metabolomics results. RESULTS: A total of 119 metabolites were identified in our experiment. The metabolic responses of B. licheniformis to acetoin stress were as follows: (i) pentose phosphate pathway and tricarboxylic acid (TCA) cycle were negatively affected by acetoin stress. In turn, glyoxylate cycle was activated to supply malic acid. (ii) Acetoin stress induced the accumulation of serine, valine, leucine and protective osmolytes (glycine and proline). (iii) Acetoin stress induced a higher saturated fatty acid ratio, which indicated a lower fluidity of cell membrane that could inhibit the entry of acetoin into cytoplasm. (iv) Synthesis of phosphatidylserine was enhanced, and phosphatidylethanolamine content was probably increased under acetoin stress. CONCLUSIONS: This study revealed the metabolic perturbations of B. licheniformis to acetoin stress. In response to acetoin stress, glyoxylate cycle was activated, protective osmolytes were accumulated, saturated fatty acid ratio was elevated and synthesis of phosphatidylserine was enhanced in B. licheniformis.
Authors: B van Ravenzwaay; G Coelho-Palermo Cunha; E Leibold; R Looser; W Mellert; A Prokoudine; T Walk; J Wiemer Journal: Toxicol Lett Date: 2007-05-25 Impact factor: 4.372
Authors: Mohamed N Triba; Laurence Le Moyec; Roland Amathieu; Corentine Goossens; Nadia Bouchemal; Pierre Nahon; Douglas N Rutledge; Philippe Savarin Journal: Mol Biosyst Date: 2014-11-10
Authors: Lloyd W Sumner; Alexander Amberg; Dave Barrett; Michael H Beale; Richard Beger; Clare A Daykin; Teresa W-M Fan; Oliver Fiehn; Royston Goodacre; Julian L Griffin; Thomas Hankemeier; Nigel Hardy; James Harnly; Richard Higashi; Joachim Kopka; Andrew N Lane; John C Lindon; Philip Marriott; Andrew W Nicholls; Michael D Reily; John J Thaden; Mark R Viant Journal: Metabolomics Date: 2007-09 Impact factor: 4.290