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Proc Natl Acad Sci U S A. 2017 Nov 28;114(48):E10389-E10398. doi: 10.1073/pnas.1711408114. Epub 2017 Nov 14.

Dual function for Tango1 in secretion of bulky cargo and in ER-Golgi morphology.

Author information

1
Directors' Research Unit, European Molecular Biology Laboratory, 69117 Heidelberg, Germany.
2
Institute of Genetics, University of Cologne, 50674 Cologne, Germany.
3
Directors' Research Unit, European Molecular Biology Laboratory, 69117 Heidelberg, Germany; mleptin@uni-koeln.de.

Abstract

Tango1 enables ER-to-Golgi trafficking of large proteins. We show here that loss of Tango1, in addition to disrupting protein secretion and ER/Golgi morphology, causes ER stress and defects in cell shape. We find that the previously observed dependence of smaller cargos on Tango1 is a secondary effect. If large cargos like Dumpy, which we identify as a Tango1 cargo, are removed from the cell, nonbulky proteins reenter the secretory pathway. Removal of blocking cargo also restores cell morphology and attenuates the ER-stress response. Thus, failures in the secretion of nonbulky proteins, ER stress, and defective cell morphology are secondary consequences of bulky cargo retention. By contrast, ER/Golgi defects in Tango1-depleted cells persist in the absence of bulky cargo, showing that they are due to a secretion-independent function of Tango1. Therefore, maintenance of ER/Golgi architecture and bulky cargo transport are the primary functions for Tango1.

KEYWORDS:

ER stress; ERES; ERGIC; GM130; Sec16

PMID:
29138315
PMCID:
PMC5715762
DOI:
10.1073/pnas.1711408114
[Indexed for MEDLINE]
Free PMC Article

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