进化相关的宿主和微生物通路调节C. elegans中的脂肪脱
Bennett W Fox1, Maximilian J Helf1, Russell N Burkhardt1
1Boyce Thompson Institute and Department of Chemistry and Chemical Biology, Cornell University, Ithaca, NY, 14853, USA.
Nature communications
|February 19, 2024
概括
肠道细菌和宿主中的小分子通过NHR-49/PPARα通路调节脂肪酸脱. 这些信号,包括细菌的becyp#1和内源的bemeth#1,控制C. elegans的脂质代谢.
科学领域:
- 脂质代谢 脂质代谢是什么
- 分子生物学分子生物学
- 微生物学 微生物学
背景情况:
- 脂肪酸脱对于metazoan膜脂质和信号分子至关重要.
- 营养和微生物群调节脱酶表达的机制在很大程度上是未知的.
研究的目的:
- 阐明内源性和微生物群依赖的信号通过C. elegans的NHR-49/PPARα通路调节脂质脱的机制.
主要方法:
- 在C. elegansβ-氧化突变体 (acdh-11) 上利用非向代谢.
- 研究了环胺合成酶在细菌becyp#1生物合成中的作用.
- 对模仿becyp#1活动的内源代谢物进行选,识别β-甲基脂肪酸 (bemeth#1).
- 对becyp#1和bemeth#1.1分析了不同的代谢途径 (β-氧化与α-氧化).
主要成果:
- 鉴定出β-cyclopropyl脂肪酸 (becyp#1) 在acdh-11突变体中积累,通过NHR-49.9激活脂肪-7表达.
- 已证明becyp#1生物合成依赖于细菌环氨酸合成酶.
- 发现了源自fcmt-1的内源贝梅特#1,模仿了becyp#1的活动.
- 显示了贝西普#1 (β-氧化) 和贝梅斯#1 (α-氧化) 的不同的代谢命运.
结论:
- 内生和微生物群衍生的信号汇聚在NHR-49/PPARα上,以调节脂肪酸脱.
- 主体和微生物群中的进化相关途径协调脂质代谢.
- 类似的信号分子的明显代谢处理突出了复杂的调节网络.
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