Yan Xuefeng, Zhou Yuhong, Liu Songwei, Gu Congwei, Xiao Wudian, Zhao Mingde, Yu Zehui, He Lvqin
School of Physical Education, Southwest Medical University, Luzhou, China.
School of Pharmacy, Southwest Medical University, Luzhou, China.
Front Microbiol. 2025 Aug 29;16:1637383. doi: 10.3389/fmicb.2025.1637383. eCollection 2025.
() causes agent Glässer's disease in swine. This study investigated the mechanism of QseC in .
The study utilized transcriptomic and metabolomic sequencing techniques. The Δ mutant was examined using transmission electron microscopy.
Transmission electron microscopy revealed that Δ mutant exhibited cell wall dissolution and cytoplasmic rarefaction, indicating membrane homeostasis disruption. Metabolomics analysis identified 819 metabolites, with 24/36 showing significant alterations in positive/negative ion modes. KEGG enrichment indicated abnormalities in amino acid synthesis and quorum sensing. Transcriptomic revealed 663 differentially expressed genes (DEGs), including upregulated membrane synthesis genes ( and ) and downregulated virulence factors ( and ). Integrated analysis demonstrated that and formed association networks with methionine and prostaglandin metabolites.
These results establish QseC's global regulatory role in , providing insights for novel control strategies.
()导致猪感染格氏病。本研究调查了QseC在()中的作用机制。
本研究采用转录组学和代谢组学测序技术。使用透射电子显微镜检查Δ突变体。
透射电子显微镜显示,Δ突变体表现出细胞壁溶解和细胞质稀疏,表明膜稳态受到破坏。代谢组学分析鉴定出819种代谢物,其中24/36在正/负离子模式下显示出显著变化。KEGG富集表明氨基酸合成和群体感应存在异常。转录组学显示663个差异表达基因(DEG),包括上调的膜合成基因(和)和下调的毒力因子(和)。综合分析表明,和与蛋氨酸和前列腺素代谢物形成关联网络。
这些结果确立了QseC在()中的全局调控作用,为新型控制策略提供了见解。