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Evidence for a COP-I-independent transport route from the Golgi complex to the endoplasmic reticulum

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UNSPECIFIED (1999) Evidence for a COP-I-independent transport route from the Golgi complex to the endoplasmic reticulum. Nature, 1 (7). pp. 423-430.

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Abstract

The cytosolic coat-protein complex COP-I interacts with cytoplasmic 'retrieval' signals present in membrane proteins that cycle between the endoplasmic reticulum (ER) and the Golgi complex, and is required for both anterograde and retrograde transport in the secretory pathway, Here we study the role of COP-I in Golgi-to-ER transport of several distinct marker molecules. Microinjection of anti-COP-I antibodies inhibits retrieval of the lectin-like molecule ERGIC-53 and of the KDEL receptor from the Golgi to the ER, Transport to the ER of protein toxins, which contain a sequence that is recognized by the KDEL receptor, is also inhibited, In contrast, microinjection of anti-COP-I antibodies or expression of a GTP-restricted Arf-l mutant does not interfere with Golgi-to-ER transport of Shiga toxin/Shiga-like toxin-1 or with the apparent recycling to the ER of Golgi-resident glycosylation enzymes. Overexpression of a GDP-restricted mutant of Rab6 blocks transport to the ER of Shiga toxin/Shiga-like toxin-1 and glycosylation enzymes, but not of ERGIC-53, the KDEL receptor or KDEL-containing toxins. These data indicate the existence of at least two distinct pathways for Golgi-to-ER transport, one COP-I dependent and the other COP-I independent. The COP-I-independent pathway is specifically regulated by Rab6 and is used by Golgi glycosylation enzymes and Shiga toxin/Shiga-like toxin-1.

Item Type: Journal Article
Subjects: Q Science > QH Natural history > QH301 Biology
Journal or Publication Title: Nature
Publisher: MACMILLAN MAGAZINES LTD
ISSN: 1465-7392
Official Date: November 1999
Dates:
DateEvent
November 1999UNSPECIFIED
Volume: 1
Number: 7
Number of Pages: 8
Page Range: pp. 423-430
Publication Status: Published

Data sourced from Thomson Reuters' Web of Knowledge

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