Abstract
BackgroundProgrammed cell death (PCD) induced by acetic acid, the main by-product released during cellulosic hydrolysis, cast a cloud over lignocellulosic biofuel fermented by Saccharomyces cerevisiae and became a burning problem. Atg22p, an ignored integral membrane protein located in vacuole belongs to autophagy-related genes family; prior study recently reported that it is required for autophagic degradation and efflux of amino acids from vacuole to cytoplasm. It may alleviate the intracellular starvation of nutrition caused by Ac and increase cell tolerance. Therefore, we investigate the role of atg22 in cell death process induced by Ac in which attempt is made to discover new perspectives for better understanding of the mechanisms behind tolerance and more robust industrial strain construction.ResultsIn this study, we compared cell growth, physiological changes in the absence and presence of Atg22p under Ac exposure conditions. It is observed that disruption and overexpression of Atg22p delays and enhances acetic acid-induced PCD, respectively. The deletion of Atg22p in S. cerevisiae maintains cell wall integrity, and protects cytomembrane integrity, fluidity and permeability upon Ac stress by changing cytomembrane phospholipids, sterols and fatty acids. More interestingly, atg22 deletion increases intracellular amino acids to aid yeast cells for tackling amino acid starvation and intracellular acidification. Further, atg22 deletion upregulates series of stress response genes expression such as heat shock protein family, cell wall integrity and autophagy.ConclusionsThe findings show that Atg22p possessed the new function related to cell resistance to Ac. This may help us have a deeper understanding of PCD induced by Ac and provide a new strategy to improve Ac resistance in designing industrial yeast strains for bioethanol production during lignocellulosic biofuel fermentation.
Highlights
Programmed cell death (PCD) induced by acetic acid, the main by-product released during cellulosic hydrolysis, cast a cloud over lignocellulosic biofuel fermented by Saccharomyces cerevisiae and became a burning problem
Atg22 deletion has a pro‐survival role during acetic acid treatment In order to assess the effects of acetic acid on cell growth and viability, the growth curves were obtained by measuring OD600, and cell viability was tested by counting colony-forming units
The mutant showed a slower cell growth than WT in synthetic complete medium (SC) without acetic acid (CK), but Atg22Δ cells seemed to be growing more quickly than BY4742 until about 10 h after acetic acid (Ac) treatment, which was presented in the insert picture
Summary
Programmed cell death (PCD) induced by acetic acid, the main by-product released during cellulosic hydrolysis, cast a cloud over lignocellulosic biofuel fermented by Saccharomyces cerevisiae and became a burning problem. Atg22p, an ignored integral membrane protein located in vacuole belongs to autophagy-related genes family; prior study recently reported that it is required for autophagic degradation and efflux of amino acids from vacuole to cytoplasm. It may alleviate the intracellular starvation of nutrition caused by Ac and increase cell tolerance. Growing exhaustion of fossil fuel and increasing deterioration of environment shine a spotlight on cellulosic ethanol which is regarded as the most promising substitute of petrochemical resources for their abundant, available, low-cost feedstocks from forestry residues, agricultural residues and energy crops [1, 2] Toxic compounds such as weak acid, furans, phenolic compounds, and hydroxymethylfurfural (HMF), which were produced during lignocellulose-based saccharification and. Further in-depth research is indispensable for understanding the mechanisms of stress tolerance, and implementing efficient and economical strategies that used S. cerevisiae as microbial factories to fabricate bioethanol
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