Mutant with diphtheria toxin receptor and acidification function but defective in entry of toxin |
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| Institution: | 1. National Institute for Basic Biology, Myodaiji-cho, Okazaki, Aichi 444, Japan;2. Institute for Molecular and Cellular Biology, Osaka University, 13 Yamada-oka, Suita, Osaka 565, Japan;1. Department of Cardiology, Cardiovascular Center, Henan Key Laboratory of Hereditary Cardiovascular Diseases, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China;2. Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, National Clinical Research Centre for Cardiovascular Diseases, No. 2 Beijing Anzhen Road, Chaoyang District, Beijing 100029, China;1. Department of Neurology, Fujian Medical University Union Hospital, Fuzhou, China;2. Department of Orthopedics, Fujian Medical University Union Hospital, Fuzhou, China;3. Institute of Clinical Neurology, Fujian Medical University, Fuzhou, China;4. Department of Neurology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China;1. Institute of Dermatology and Venereology, Dermatology Hospital, Southern Medical University, Guangzhou, China;2. Department of Dermatology, The First People''s Hospital of Foshan, Foshan, China;3. Department of Dermatology, Dermatology Hospital, Southern Medical University, Guangzhou, China;4. Guangdong-Hong Kong Joint Laboratory of Dermatology Research, Guangzhou, China |
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| Abstract: | A mutant of Chinese hamster ovary cells, GE1, that is highly resistant to diphtheria toxin was isolated. The mutant contains 50% ADP-ribosylatable elongation factor 2, but its protein synthesis was not inhibited by the toxin even at concentrations above 100 μg/ml. 125I-labeled diphtheria toxin was associated with GE1 cells as well as with the parent cells but did not block protein synthesis of GE1 cells even when the cells were exposed to low pH in the presence or absence of NH4Cl. The infections of GE1 cells and the parent cells by vesicular stomatitis virus were similar. GE1 cells were cross-resistant to Pseudomonas aeruginosa exotoxin A and so were about 1000 times more resistant to this toxin than the parent cells. Hybrids of GE1 cells and the parent cells or mutant cells lacking a functional receptor were more sensitive to diphtheria toxin than GE1 cells. These results suggest that entry of diphtheria toxin into cells requires a cellular factor(s) in addition to those involved in receptor function and acidification of endosomes and that GE1 cells do not express this cellular factor. This character is recessive in GE1 cells. |
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