Mea6 controls VLDL transport through the coordinated regulation of COPil assembly

Lipid accumulation, which may be caused by the disturbance in very low density lipoprotein （VLDL） secretion in the liver, can lead to fatty liver disease. VLDL is synthesized in endoplasmic reticulum （ER） and transported to Golgi apparatus for secretion into plasma. However, the underlying molecular...

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Bibliographic Details
Published in细胞研究：英文版 no. 7; pp. 787 - 804
Main Author Yaqing Wang Liang Liu Hongsheng Zhang Junwan Fan FengZhang Mei Yu Lei Shi Lin Yang Sin Man Lam Huimin Wang Xiaowei Chen Yingchun Wang Fei Gao Guanghou Shui Zhiheng Xu
Format Journal Article
LanguageEnglish
Published 2016
Subjects
VLDL
控制
极低密度脂蛋白
监管
细胞特异性
蛋白复合物
装配协调
运输
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Summary:Lipid accumulation, which may be caused by the disturbance in very low density lipoprotein （VLDL） secretion in the liver, can lead to fatty liver disease. VLDL is synthesized in endoplasmic reticulum （ER） and transported to Golgi apparatus for secretion into plasma. However, the underlying molecular mechanism for VLDL transport is still poor- ly understood. Here we show that hepatocyte-specific deletion of meningioma-expressed antigen 6 （Mea6）/cutaneous T cell lymphoma-associated antigen 5C （cTAGESC） leads to severe fatty liver and hypolipemia in mice. Quantitative lip- idomic and proteomic analyses indicate that Mea6/cTAGE5 deletion impairs the secretion of different types of lipids and proteins, including VLDL, from the liver. Moreover, we demonstrate that Mea6/cTAGE5 interacts with compo- nents of the ER coat protein complex II （COPII） which, when depleted, also cause lipid accumulation in hepatocytes. Our findings not only reveal several novel factors that regulate lipid transport, but also provide evidence that Mea6 plays a critical role in lipid transportation through the coordinated regulation of the COPII machinery.
Bibliography:31-1568
Mea6; fatty liver; lipid transport and VLDL secretion; COPII machinery
Lipid accumulation, which may be caused by the disturbance in very low density lipoprotein （VLDL） secretion in the liver, can lead to fatty liver disease. VLDL is synthesized in endoplasmic reticulum （ER） and transported to Golgi apparatus for secretion into plasma. However, the underlying molecular mechanism for VLDL transport is still poor- ly understood. Here we show that hepatocyte-specific deletion of meningioma-expressed antigen 6 （Mea6）/cutaneous T cell lymphoma-associated antigen 5C （cTAGESC） leads to severe fatty liver and hypolipemia in mice. Quantitative lip- idomic and proteomic analyses indicate that Mea6/cTAGE5 deletion impairs the secretion of different types of lipids and proteins, including VLDL, from the liver. Moreover, we demonstrate that Mea6/cTAGE5 interacts with compo- nents of the ER coat protein complex II （COPII） which, when depleted, also cause lipid accumulation in hepatocytes. Our findings not only reveal several novel factors that regulate lipid transport, but also provide evidence that Mea6 plays a critical role in lipid transportation through the coordinated regulation of the COPII machinery.
ISSN:1001-0602
1748-7838