Abstract
Cholera toxin (CT) follows a glycolipid-dependent entry pathway from the plasma membrane through the trans-Golgi network (TGN) to the endoplasmic reticulum (ER) where it is retro-translocated into the cytosol to induce toxicity. Whether access to the Golgi apparatus is necessary for transport to the ER is not known. Exo2 is a small chemical that rapidly blocks anterograde traffic from the ER to the Golgi and selectively disrupts the Golgi apparatus but not the TGN. Here we use Exo2 to determine the role of the Golgi apparatus in CT trafficking. We find that under the condition of complete Golgi ablation by Exo2, CT reaches the TGN and moves efficiently into the ER without loss in toxicity. We propose that even in the absence of Exo2 the glycolipid pathway that carries the toxin from plasma membrane into the ER bypasses the Golgi apparatus entirely.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Benzaldehydes / pharmacology*
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Cell Line
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Cell Membrane / drug effects
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Cell Membrane / physiology*
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Cholera Toxin / analysis
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Cholera Toxin / metabolism*
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Colforsin / pharmacology
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Electric Conductivity
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Endoplasmic Reticulum / physiology*
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Glycoproteins / analysis
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Golgi Apparatus / chemistry
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Golgi Apparatus / drug effects
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Golgi Apparatus / physiology
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Protein Transport / drug effects
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Protein Transport / physiology
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Pyrimidines / pharmacology*
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Receptors, Peptide / analysis
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trans-Golgi Network / chemistry
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trans-Golgi Network / drug effects
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trans-Golgi Network / physiology*
Substances
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4-hydroxy-3-methoxy-(5,6,7,8-tetrahydro(1)benzothieno(2,3-d)pyrimidin-4-yl)hydrazone benzaldehyde
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Benzaldehydes
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Glycoproteins
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KDEL receptor
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Pyrimidines
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Receptors, Peptide
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Colforsin
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Cholera Toxin