TANGO1 and Mia2/cTAGE5 (TALI) cooperate to export bulky pre-chylomicrons/VLDLs from the endoplasmic reticulum

António J M Santos; Cristina Nogueira; Maria Ortega-Bellido; Vivek Malhotra

doi:10.1083/jcb.201603072

TANGO1 and Mia2/cTAGE5 (TALI) cooperate to export bulky pre-chylomicrons/VLDLs from the endoplasmic reticulum

J Cell Biol. 2016 May 9;213(3):343-54. doi: 10.1083/jcb.201603072. Epub 2016 May 2.

Authors

António J M Santos¹, Cristina Nogueira¹, Maria Ortega-Bellido¹, Vivek Malhotra²

Affiliations

¹ Centre for Genomic Regulation, The Barcelona Institute of Science and Technology, 08003 Barcelona, Spain Universitat Pompeu Fabra, 08002 Barcelona, Spain.
² Centre for Genomic Regulation, The Barcelona Institute of Science and Technology, 08003 Barcelona, Spain Universitat Pompeu Fabra, 08002 Barcelona, Spain Institució Catalana de Recerca i Estudis Avançats, 08010 Barcelona, Spain vivek.malhotra@crg.eu.

Abstract

Procollagens, pre-chylomicrons, and pre-very low-density lipoproteins (pre-VLDLs) are too big to fit into conventional COPII-coated vesicles, so how are these bulky cargoes exported from the endoplasmic reticulum (ER)? We have shown that TANGO1 located at the ER exit site is necessary for procollagen export. We report a role for TANGO1 and TANGO1-like (TALI), a chimeric protein resulting from fusion of MIA2 and cTAGE5 gene products, in the export of pre-chylomicrons and pre-VLDLs from the ER. TANGO1 binds TALI, and both interact with apolipoprotein B (ApoB) and are necessary for the recruitment of ApoB-containing lipid particles to ER exit sites for their subsequent export. Although export of ApoB requires the function of both TANGO1 and TALI, the export of procollagen XII by the same cells requires only TANGO1. These findings reveal a general role for TANGO1 in the export of bulky cargoes from the ER and identify a specific requirement for TALI in assisting TANGO1 to export bulky lipid particles.

MeSH terms

Antigens, Neoplasm / genetics
Antigens, Neoplasm / metabolism
Antigens, Neoplasm / physiology*
Apolipoproteins B / metabolism
Aryl Hydrocarbon Receptor Nuclear Translocator / genetics
Aryl Hydrocarbon Receptor Nuclear Translocator / metabolism
Aryl Hydrocarbon Receptor Nuclear Translocator / physiology*
Autophagy
Caco-2 Cells
Collagen / metabolism
Endoplasmic Reticulum / metabolism*
Gene Deletion
Hep G2 Cells
Humans
Lipid Metabolism*
Lipoproteins, VLDL / metabolism
Models, Biological
Models, Molecular
Mutant Chimeric Proteins / metabolism
Neoplasm Proteins / genetics
Neoplasm Proteins / metabolism
Neoplasm Proteins / physiology*
Protein Transport / physiology
Tumor Suppressor Proteins / genetics
Tumor Suppressor Proteins / metabolism
Tumor Suppressor Proteins / physiology*

Substances

ARNT protein, human
Antigens, Neoplasm
Apolipoproteins B
Lipoproteins, VLDL
MIA2 protein, human
Mutant Chimeric Proteins
Neoplasm Proteins
Tumor Suppressor Proteins
Aryl Hydrocarbon Receptor Nuclear Translocator
Collagen