Stearic acid represents one of the most abundant fatty acids in the Western diet and profoundly regulates health and diseases of animals and human beings. We previously showed that stearic acid supplementation promoted development of the terrestrial model nematodeCaenorhabditis elegansin chemically defined CeMM food environment. However, whether stearic acid regulates development of other nematodes remains unknown. Here, we found that dietary supplementation with stearic acid could promote the development of the marine nematodeLitoditis marina, belonging to the same family asC. elegans, indicating the conserved roles of stearic acid in developmental regulation. We further employed transcriptome analysis to analyze genome-wide transcriptional signatures ofL. marinawith dietary stearic acid supplementation. We found that stearic acid might promote development ofL. marinavia upregulation of the expression of genes involved in aminoacyl-tRNA biosynthesis, translation initiation and elongation, ribosome biogenesis, and transmembrane transport. In addition, we observed that the expression of neuronal signaling-related genes was decreased. This study provided important insights into how a single fatty acid stearic acid regulates development of marine nematode, and further studies with CRISPR genome editing will facilitate demonstrating the molecular mechanisms underlying how a single metabolite regulates animal development and health.Keywords:marine nematode;stearic acid;CeMM;development;transcriptome;protein translation;neuronal signaling
Cao Xuwen,Xie Yusu,Yang Hanwen,Sun Peiqi,Xue Beining,Garcia L. Rene,Zhang Liusuo
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 β-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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