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EAT-2 attenuates C. elegans development via metabolic remodeling in a chemically defined food environment.
Cao, Xuwen; Xie, Yusu; Yang, Hanwen; Sun, Peiqi; Xue, Beining; Garcia, L Rene; Zhang, Liusuo.
Afiliación
  • Cao X; CAS and Shandong Province Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, 266071, Qingdao, China.
  • Xie Y; Laboratory of Marine Biology and Biotechnology, Qingdao National Laboratory for Marine Science and Technology, 266237, Qingdao, China.
  • Yang H; Center for Ocean Mega-Science, Chinese Academy of Sciences, 7 Nanhai Road, 266071, Qingdao, China.
  • Sun P; University of Chinese Academy of Sciences, 100049, Beijing, China.
  • Xue B; Institute of Marine Science and Technology, Shandong University, 72 Binhai Road, 266237, Qingdao, China.
  • Garcia LR; CAS and Shandong Province Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, 266071, Qingdao, China.
  • Zhang L; Laboratory of Marine Biology and Biotechnology, Qingdao National Laboratory for Marine Science and Technology, 266237, Qingdao, China.
Cell Mol Life Sci ; 80(8): 205, 2023 Jul 14.
Article en En | MEDLINE | ID: mdl-37450052
Dietary intake and nutrient composition regulate animal growth and development; however, the underlying mechanisms remain elusive. Our previous study has shown that either the mammalian deafness homolog gene tmc-1 or its downstream acetylcholine receptor gene eat-2 attenuates Caenorhabditis elegans development in a chemically defined food CeMM (C. elegans maintenance medium) environment, but the underpinning mechanisms are not well-understood. Here, we found that, in CeMM food environment, for both eat-2 and tmc-1 fast-growing mutants, several fatty acid synthesis and elongation genes were highly expressed, while many fatty acid ß-oxidation genes were repressed. Accordingly, dietary supplementation of individual fatty acids, such as monomethyl branch chain fatty acid C17ISO, palmitic acid and stearic acid significantly promoted wild-type animal development on CeMM, and mutations in either C17ISO synthesis gene elo-5 or elo-6 slowed the rapid growth of eat-2 mutant. Tissue-specific rescue experiments showed that elo-6 promoted animal development mainly in the intestine. Furthermore, transcriptome and metabolome analyses revealed that elo-6/C17ISO regulation of C. elegans development may be correlated with up-regulating expression of cuticle synthetic and hedgehog signaling genes, as well as promoting biosynthesis of amino acids, amino acid derivatives and vitamins. Correspondingly, we found that amino acid derivative S-adenosylmethionine and its upstream metabolite methionine sulfoxide significantly promoted C. elegans development on CeMM. This study demonstrated that C17ISO, palmitic acid, stearic acid, S-adenosylmethionine and methionine sulfoxide inhibited or bypassed the TMC-1 and EAT-2-mediated attenuation of development via metabolic remodeling, and allowed the animals to adapt to the new nutritional niche.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Nutrientes / Receptores Nicotínicos / Caenorhabditis elegans / Proteínas de Caenorhabditis elegans / Ácidos Grasos Límite: Animals Idioma: En Revista: Cell Mol Life Sci Asunto de la revista: BIOLOGIA MOLECULAR Año: 2023 Tipo del documento: Article País de afiliación: China Pais de publicación: Suiza
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Nutrientes / Receptores Nicotínicos / Caenorhabditis elegans / Proteínas de Caenorhabditis elegans / Ácidos Grasos Límite: Animals Idioma: En Revista: Cell Mol Life Sci Asunto de la revista: BIOLOGIA MOLECULAR Año: 2023 Tipo del documento: Article País de afiliación: China Pais de publicación: Suiza