Negative effects characterization and comparative transcriptomics elucidation on the lag phase of an industrial S. cerevisiae under the corn stover hydrolysate stress

• Published in: bioRxiv
• Main Authors: Kuang, Xiaolin, Guo, Yaping, Zhang, Zhengyue, Hu, Xiangdong, Han, Xuebing, Ouyang, Yidan, Xiao, Difan, Li, Qian, Wang, Hanyu, Li, Xi, Chen, Qiang, Ma, Menggen
• Format: Paper
• Language: English
• Published: Cold Spring Harbor Cold Spring Harbor Laboratory Press 18.03.2020
• Subjects: Biofuels; Biosynthesis; Detoxification; Endoplasmic reticulum; Ergosterol; Exploration; Fermentation; Gene expression; Glutaredoxin; Heat shock proteins; Kinases; Lag phase; Lignocellulose; MAP kinase; Metabolism; Mitochondria; Osmotic stress; Oxidative stress; Oxidoreductase; Protein kinase; Reactive oxygen species; Saccharomyces cerevisiae; Signal transduction; Sulfur; Thioredoxin; Toxicity; Transcription factors; Yeast
• DOI: 10.1101/2020.03.16.994723

During biofuels fermentation from pretreated lignocellulosic biomass, the strong toxicity of the lignocellulose hydrolysate is resulted from the synergistic effect of multiple lignocellulosic inhibitors, which far exceeds the sum of effects caused by every single inhibitor. Meanwhile, the synergistic effect is unclear and the underlying response mechanism of the industrial yeast towards the actual pretreated lignocellulose hydrolysate is still under exploration. Here, we employed an industrial S. cerevisiae for the transcriptomic analysis in two time points (early and late) of the lag phase under the corn stover hydrolysate stress. As investigation, the corn stover hydrolysate caused the accumulation of reactive oxygen species (ROS), damages of mitochondrial membrane and endoplasmic reticulum (ER) membrane in the industrial S. cerevisiae YBA_08 during the lag phase, especially these negative effects were more significant at the early lag phase. Based on the transcriptome profile, the industrial S. cerevisiae YBA_08 might recruit stress-related transcription factors (MSN4, STE12, SFL1, CIN5, COM2, MIG3, etc.) through the mitogen-activated protein kinase (MAPK)-signaling pathway to induce a transient G1/G2 arrest, and to activate defense bioprocesses like protectants metabolism, sulfur metabolism, glutaredoxin system, thioredoxin system, heat shock proteins chaperone and oxidoreductase detoxification, resisting those compounded stresses including oxidative stress, osmotic stress and structural stress. Surprisingly, this defense system might be accompanied with the transient repression of several bioprocesses like fatty acid metabolism, purine de novo biosynthesis and ergosterol biosynthesis.