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J. Cell Biol.,
Volume 143, Number 3, November 2, 1998 601-612
* Abteilung Klinische Biochemie, Universität Göttingen, D-37070 Göttingen, Germany; A cholera toxin mutant (CTX-K63) unable
to raise cAMP levels was used to study in Vero cells
the retrograde transport of the toxin A subunit (CTX-A-K63), which possesses a COOH-terminal KDEL retrieval signal. Microinjected GTP- Institut für Biochemie I, University of
Heidelberg, D-69120 Heidelberg, Germany; § European Molecular Biology Laboratory, D-69012 Heidelberg, Germay; IRIS,
The Chiron Vaccines Immunobiological Research Institute, Via Fiorentina, I-53100 Siena, Italy; and ¶ Max-Planck-Institut für
Biophysikalische Chemie, D-37077 Göttingen, Germany
-S inhibits the internalization as well as Golgi-ER transport of CTX-A-K63. The appearance of CTX-A-K63 in the Golgi
induces a marked dispersion of Erd2p and p53 but not
of the Golgi marker giantin. Erd2p is translocated under these conditions most likely to the intermediate
compartment as indicated by an increased colocalization of Erd2p with mSEC13, a member of the mammalian coat protein II complex. IgGs as well as Fab fragments directed against Erd2p, 
-COP, or p23, a new member of the p24 protein family, inhibit or block retrograde transport of CTX-A-K63 from the Golgi without affecting its internalization or its transport to the
Golgi. Anti-Erd2p antibodies do not affect the binding
of CTX-A to Erd2p, but inhibit the CTX-K63-induced translocation of Erd2p and p53.
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