Contribution of sams-1 and pmt-1 to lipid homoeostasis in adult Caenorhabditis elegans

Yingxiu Li, Keun Na, Hyoung Joo Lee, Eun Young Lee, Young Ki Paik

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Abstract

Accumulation of lipids inside the cell is primarily caused by disorders of lipid metabolism. S-adenosylmethionine synthetase (SAMS) produces SAM, an important methyl donor in various phospholipid methyltransferase reactions catalysed by phosphoethanolamine N-methyltransferase (PMT-1). A gel-based, quantitative proteomic analysis of the RNA interference (RNAi)-mediated inactivation of the pod-2 gene, which encodes acetyl-CoA carboxylase, showed a substantial down-regulation of SAMS-1. Consequently, RNAi of either sams-1 or pmt-1 caused a significant increase in lipid droplet size in the intestine of Caenorhabditis elegans. Lipid droplets exhibited increased triacylglycerol (TG) and decreased phosphatidylcholine (PC) levels, suggesting a reciprocal relationship between TG and PC regulation. These lipid-associated phenotypes were rescued by choline feeding. Among the five fat metabolism-related genes examined, two genes were highly induced by inactivation of sams-1 or pmt-1: pod-2 and stearoyl-CoA desaturase (fat-7). Thus, both SAMS-1 and PMT-1 were shown to contribute to the homoeostasis of TG and PC levels in C. elegans, which would provide an important survival strategy under harsh environmental conditions. The Authors 2011. Published by Oxford University Press on behalf of the Japanese Biochemical Society. All rights reserved2011

Original languageEnglish
Pages (from-to)529-538
Number of pages10
JournalJournal of Biochemistry
Volume149
Issue number5
DOIs
Publication statusPublished - 2011 May 1

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All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology

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