双功能定数感应信号合成酶 DspII 和 DspI 是 Pseudomonas aeruginosa 病毒性转换的协调因子
Jiahui Huang1,2, Tian Zhou1,3, Xiaofan Zhou1
1Guangdong Provincial Key Laboratory of Microbial Signals and Disease Control, Integrative Microbiology Research Centre, South China Agricultural University, Guangzhou, China.
Nature communications
|January 22, 2026
概括
Pseudomonas aeruginosa 通过使用 DspII-DspI 蛋白质复合体,从慢性感染转变为急性感染. 这种复合物合成了一个信号分子,增强病毒毒性并促进急性感染特征.
科学领域:
- 微生物学 微生物学
- 细菌病原体的产生
- 检验委员会检测检验委员会检测.
背景情况:
- 细菌在急性和慢性感染之间过渡,影响宿主生存.
- 宿主和环境因素影响这种过渡,但细菌的自我调节尚不清楚.
研究的目的:
- 为了确定活跃调节急性和慢性感染状态之间的切换的细菌因素.
- 阐明 Pseudomonas aeruginosa 调节其毒性过渡的机制.
主要方法:
- 新型伊诺伊尔-CoA水合酶/异构酶PA0744 (DspII) 的鉴定和特征.
- 分析DspII-DspI异构复合物的形成及其在合成cis-2-decenoic acid (CDA) 中的作用.
- 研究CDA对RbdA,c-di-GMP/FleQ通路和III型分泌系统 (T3SS) 表达的下游影响.
主要成果:
- DspII与DSPI共同调节,形成一种以细胞密度依赖的方式合成CDA的复合物.
- 通过c-di-GMP/FleQ通路,CDA通过c-di-GMP/FleQ通路激活生物膜分散和蜂群运动.
- DspII-DspI复合体对抗sRNAs RsmY/RsmZ,增加T3SS的产生和急性毒性.
结论:
- DspII-DspI复合体发挥着双重作用:合成CDA和调节T3SS基因表达.
- 这代表了一种细菌自我调节机制,控制了P. aeruginosa的慢性和急性毒性之间的切换.
- CDA水平微调DspII-DspI复合体的亲和力和T3SS基因表达,突出了一个复杂的调节循环.
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