时间标签：数据日期 2026-11-03 · 生成时间 2026-11-03 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/31 – 2026/11/03 ｜ 情报发生日期 2026-11-03
研究问题
We assessed whether RNAi-mediated depletion of rict-1 phe- nocopied the null allele used in this study, rict-1(ft7).；Given that RICT-1 functions as an essential component of mTORC2, we next assessed whether depletion of another core mTORC2 subunit, SINH-1, yields similar dietary sensitivity.；To determine whether this dietary modulation is specific to mTORC2, we next depleted the catalytic subunit of mTORC1, daf-15/ raptor.
方法
To further validate the RNAi-based findings, we analyzed the rict-1(ft7);metr-1(syb11628) double mutant.；To test this, we performed targeted metabolomic profil- ing of key Met-C intermediates [Hcy, Met, S-adenosylmethionine (SAM), and S-adenosylhomocysteine (SAH)] in wild-type and rict-1(-) worms grown on either OP50 or HT115.；To determine whether differences in amino acid availability might account for these effects, we performed targeted bacterial metabo- lomics on OP50, HT115, and BW25113.
核心结论
In this study, we show that the C. elegans RICT-1 is a part of a gene- diet interaction that maintains adaptive capacity to diets with different B12 content.；Here, we show that the rict-1 mutant grown on a high B12 diet engages Met-C as well as the transsulfuration and the canonical propionate catabolic pathways.；Inter- estingly, we show that the bacterial diet supplies both B12 as well as the essential amino acid methionine (Met) to augment succinate produc- tion, mitochondrial fragmentation, mitophagy, and promote stress tolerance and longevity.
局限
However, in some genetic mutants studied in laboratories, variations in lifespan or other phenotypes become apparent only on specific diets, thereby giving us a window of opportunity to understand how diet-gene interactions maintain normal lifespan and how their perturbations may lead to diseases.；For example, when the alh-6 (a proline catabolism gene) mutant is fed the high proline-containing E. coli OP50 diet, it cannot convert the proline-5-carboxylate (P5C) to glutamate and fails to maintain mito- chondrial homeostasis.
对本项目的价值
中高价值：属「营养感知—自噬—蛋白稳态轴」方向；线粒体功能与氧化应激栏目可用作本项目文献库与综述素材。 ｜ 价值分 3.0/5（★★★☆☆）
全文来源
出版商/仓储 OA PDF（正文 116,818 字符，题名指纹 0.92，已过 DOI 逐字 + 题名指纹 + 正文长度三重归属校验）
原文题录
- 中文题名：RICTOR 经甲硫氨酸循环—线粒体自噬轴调控跨物种互作并影响寿命
- 英文标题：RICTOR regulates an interspecies crosstalk that influences longevity through a methionine cycle-mitophagy axis.
- 期刊与标识：Nat Commun · PMID 42967947 · DOI 10.1038/s41467-026-77722-7 · EDAT 2026-11-01