瑞克托 (RICTOR) 调节了一种跨物种交叉声调节,通过一种新的甲氨酸循环-甲基菌轴影响长寿
Simran Motwani1, Somya Bhandari1, Shivani Chitkara2
1Molecular Aging Laboratory, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi 110067, India.
bioRxiv : the preprint server for biology
|August 12, 2025
概括
拉巴胺素复合体2 (mTORC2) 组成部分RICTOR的机械性标调节了对维生素B12的反应中饮食可塑性. 失去RICTOR可以通过将叶酸-氨酸循环与线粒细胞衰变联系起来,从而提高应激耐受性和寿命.
科学领域:
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
- 代谢过程中的代谢.
背景情况:
- 生物体的健康取决于使生理特征适应环境变化,特别是饮食.
- 基因-饮食相互作用是关键的,但微生物代谢物和宿主途径之间的分子联系尚未得到充分探索.
研究的目的:
- 鉴定饮食可塑性的调节者,以应对微生物代谢产物.
- 研究RICTOR在将营养信号与宿主应激反应和新陈代谢相结合方面的作用.
主要方法:
- 使用*Caenorhabditis elegans*作为一个模型生物.
- 研究了涉及维生素B12和RICTOR的基因饮食相互作用.
- 分析了依赖于B12的酶 (甲氨酸合成酶,甲基马洛尼尔-CoA突变酶) 和它们的下游效应.
主要成果:
- 在维生素B12丰富的饮食中,失去*rict-1* (RICTOR ortholog) 增强了透应激耐受性和寿命.
- 现型适应需要 metionin 合成酶和甲基马洛尼尔-CoA 突变酶.
- 从酸代谢中提升的酸盐会诱导髓,这对应激弹性和寿命至关重要.
- 甲氨酸合成酶-甲基菌轴是由微生物维生素B12和甲氨酸调节的.
结论:
- 瑞克托抑制宿主对微生物代谢物的敏感性,维持线粒体平衡,调节寿命.
- RICTOR通过器官质量控制,在隔离宿主生理学免受营养驱动的干扰方面发挥着关键作用.
- 通过RICTOR和线粒细胞衰变,确定了一条连接微生物代谢物,宿主代谢和寿命的保存途径.
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