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

UNLABELLED

To investigate the mechanism of osmotic stress produced by 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, suppressed the synthesis of l -homoserine and instead enhanced its catabolic activity. In response to osmotic stress, 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 's tolerance to l-homoserine stress during amino-acid fermentation and highlight potential targets for metabolic engineering strategies.

SUPPLEMENTARY INFORMATION

The online version contains supplementary material available at 10.1007/s13205-025-04304-7.