细菌酸甘氨酸作为消化信号,调解宿主适应C. elegans的各种食物资源
Fanrui Hao1, Huimin Liu1, Bin Qi2
1Southwest United Graduate School, Yunnan Key Laboratory of Cell Metabolism and Diseases, State Key Laboratory of Conservation and Utilization of Bio-resources in Yunnan, Center for Life Sciences, School of Life Sciences, Yunnan University, Kunming, China.
Nature communications
|April 16, 2024
概括
细菌甘油 (PGN) 信号好食物,通过BCF-1相互作用激活消化. 这种相互作用抑制了线粒体展开蛋白反应 (UPRmt),通过使动物能够食用各种食物来增强动物的适应性.
科学领域:
- 动物生理学 动物生理学
- 微生物学 微生物学
- 遗传学 是一个遗传学.
背景情况:
- 食物的可用性对于动物的生存和适应至关重要.
- 对于各种食物摄入来说,激活宿主消化的特定信号在很大程度上是未知的.
- 该C. elegans模型提供了对宿主微生物相互作用和消化过程的见解.
研究的目的:
- 为了识别激活动物消化消耗各种食物的信号.
- 阐明细菌成分影响宿主消化过程的分子机制.
- 了解消化,适应和生存之间的联系.
主要方法:
- 利用C. elegans模型系统研究食物消化.
- 研究了细菌甘油 (PGN) 作为食物信号的作用.
- 鉴定了细菌殖民因子-1 (BCF-1) 和它与PGN的相互作用.
- 研究了线粒体未折叠蛋白反应 (UPRmt) 和p38 MAPK/PMK-1通路的调节.
主要成果:
- 细菌PGN作为一个独特的信号来激活不可食用的食物的消化.
- BCF-1与PGN相互作用,通过调节神经类蛋白 (NLP-3) 来抑制UPRmt.
- UPRmt的激活阻碍了食物消化,这取决于p38 MAPK/PMK-1通路;抑制PMK-1可以挽救bcf-1突变者的消化缺陷.
结论:
- PGN-BCF-1相互作用作为"好食物信号",促进消化和生长.
- 这种信号通路通过扩大可消费食物的范围来增强宿主适应.
- 有效的消化对于动物在自然环境中的适应能力至关重要.
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