Affiliation:
1. College of Food Science and Technology, Yunnan Agricultural University, Kunming 650201, China
2. Center for Life Sciences, School of Life Sciences, Yunnan University, Kunming, Yunnan 650091, China
Abstract
Abstract
Zinc is one of the most important trace elements as it plays a vital role in many biological processes. As well, aberrant zinc metabolism has been implicated in lipid-related metabolic diseases. Previously, we showed that zinc antagonizes iron to regulate sterol regulatory element-binding proteins and the stearoyl-CoA desaturase (SREBP-SCD) pathway in lipid metabolism in the model organism Caenorhabditis elegans. In this study, we present the identification of another cation diffusion facilitator, CDF-1, which regulates lipid metabolism along with SUR-7 in response to zinc. Inactivation of SBP-1, the only homolog of SREBPs, leads to an increased zinc level but decreased lipid accumulation. However, either the cdf-1(n2527) or sur-7(tm6523) mutation could successfully restore the altered fatty acid profile, fat content, and zinc level of the sbp-1(ep79) mutant. Furthermore, we found that CDF-1/SUR-7 may functionally bypass SBP-1 to directly affect the conversion activity of SCD in the biosynthesis of unsaturated fatty acids and lipid accumulation. Collectively, these results consistently support the link between zinc homeostasis and lipid metabolism via the SREBP-SCD axis by the cation diffusion facilitators CDF-1 and SUR-7.
Funder
National Natural Science Foundation of China
Ministry of Science and Technology of the People’s Republic of China
Yunnan Applied Basic Research Projects
Yunnan Oversea High-level Talents Program
Publisher
Oxford University Press (OUP)
Subject
Genetics(clinical),Genetics,Molecular Biology
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