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<p>To investigate the mechanism of osmotic stress produced by <i>Corynebacterium glutamicum (C. glutamicum)</i> in the production of <span>l</span>-homoserine<i>.</i> The present study employed genomic and transcriptomic analyses of both evolved strains and the parental strain grown under <span>l</span>-homoserine osmotic stress to investigate the response mechanisms and identify specific tolerance targets. The results indicated that the evolved strain enhanced its tolerance to <span>l</span>-homoserine stress by inactivating aspartokinase, thereby interrupting the intracellular synthesis pathway of <span>l</span>-homoserine. Early in stress exposure, <i>C. glutamicum</i> suppressed the synthesis of <span>l</span> -homoserine and instead enhanced its catabolic activity. In response to osmotic stress, <i>C. glutamicum</i> also relied on a variety of energy metabolism and ion transport pathways, including ABC transporters and ATP metabolism, which are essential for high-osmolarity tolerance. Given the gradual accumulation of <span>l</span>-homoserine within the cell, this study focused on the transcriptional expression patterns during the adaptation phase, excluding cellular responses during the high-concentration stress phase. These findings provide valuable insights for improving <i>C. glutamicum</i>’s tolerance to <span>l</span>-homoserine stress during amino-acid fermentation and highlight potential targets for metabolic engineering strategies.</p>

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Omics studies reveal the response mechanisms of Corynebacterium glutamicum to l-homoserine osmotic stress

  • 期刊论文

  • 发表日期：

    2025年4月16日

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  • Jian Wang,
  • Yicun Lin,
  • Jian Yang,
  • Yuxiang Chen,
  • Ning Xu,
  • Jun Liu,
  • Wei Sun,
  • Dawei Li

摘要

To investigate the mechanism of osmotic stress produced by Corynebacterium glutamicum (C. glutamicum) in the production of l-homoserine. The present study employed genomic and transcriptomic analyses of both evolved strains and the parental strain grown under l-homoserine osmotic stress to investigate the response mechanisms and identify specific tolerance targets. The results indicated that the evolved strain enhanced its tolerance to l-homoserine stress by inactivating aspartokinase, thereby interrupting the intracellular synthesis pathway of l-homoserine. Early in stress exposure, C. glutamicum suppressed the synthesis of l -homoserine and instead enhanced its catabolic activity. In response to osmotic stress, C. glutamicum also relied on a variety of energy metabolism and ion transport pathways, including ABC transporters and ATP metabolism, which are essential for high-osmolarity tolerance. Given the gradual accumulation of l-homoserine within the cell, this study focused on the transcriptional expression patterns during the adaptation phase, excluding cellular responses during the high-concentration stress phase. These findings provide valuable insights for improving C. glutamicum’s tolerance to l-homoserine stress during amino-acid fermentation and highlight potential targets for metabolic engineering strategies.