| Summary: | 碩士 === 國立臺灣大學 === 分子與細胞生物學研究所 === 105 === Lipid contents are essential for developmental processes in many species. Dysregulation of lipid metabolism has been associated with many severe diseases, like obesity, cardiac dysfunction, and diabetes mellitus. Although lipid metabolism has been extensively studied, the relationship between diets, lipid content and developmental rate remains largely unknown. In our studies, we used C. elegans as the model organism and fed them bacteria Comamonas DA1877 or E. coli OP50 to investigate how diets regulate lipid content and developmental rate. Previous studies have shown that wild type worms had lower lipid content and accelerated developmental rate on DA1877 than OP50 diet. sams-1 is a S-adenosyl methionine (SAM) synthase gene which is reported to regulate lipid content. Our data revealed that, sams-1 deficiency worms exhibited high lipid content and decreased developmental rate on both diets. To understand its underlying mechanism, we supply SAM for sams-1 mutants. Results showed that SAM supplement affected lipid content and developmental rate. However a SAM supplement level could not mimic DA1877-mediated lipid reduction and developmental rate acceleration, suggesting that sams-1 has a SAM-synthesis dependent and independent role in regulation of lipid reduction and developmental rate. To understand SAM-synthesis independent pathway, we observed the localization of SAMS-1. We found that SAMS-1 is expressed in the intestinal and hypodermal cells in both diets. Specifically, SAMS-1 is localized in the nucleus of these cells. In mammals, MAT II
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