@article{91c04073d1074899b9f247a83ca6a866,
title = "Altered interaction between Sendai virus and a Chinese hamster cell mutant with defective cholesterol synthesis",
abstract = "An amphotericin B-resistant mutant (AMBr-1) isolated from the Chinese hamster V79 cell line is defective in a pathway for sterol synthesis and contains a much reduced free cholesterol level as compared with the parental V79. The character of the plasma membrane of AMBr-1 was compared with that of V79 by measuring the fusion with the envelope of the Sendai virus and also by measuring membrane fluidity: AMBr-1 was found to be more sensitive to Sendai virus-induced cytolysis than V79. Both assays for membrane-permeability change and electron spin resonance (ESR) study showed an enhanced response to the fusion between viral envelope and plasma membrane in AMBr-1 cells. Measurement of the fluorescence polarization for 1,6-diphenyl-1,3,5-hexatriene suggested that the membrane of AMBr-1 was more fluid than that of V79. This aberrant nature of the cell membrane of AMBr-1 might be caused by the altered membranous sterol content.",
keywords = "(Chinese hamster cell), Amphotericin B, Cholesterol synthesis, Membrane fluidity, Membrane fusion, Sendai virus",
author = "Akihiko Yoshimura and Toshihide Kobayashi and Katsuhiko Hidaka and Michihiko Kuwano and Ohnishi, {Shun ichi}",
note = "Funding Information: cholesterol was not required for the lytic response of ganglioside-containing liposome induced by Sendai virus, and also that the presence of cholesterol suppressed the leakage response• They suggested the presence of cholesterol in the target membrane may positively or negatively modulate the m0tmbrane leakage induced by Sendai virus, depending on the lipid composition or the viral receptor (glycoprotein or ganglioside) in the target membrane. In our present study, we have employed two isogenic cell lines with low and high sterol contents to question the requirement of cholesterol for the fusion process in cultured living cells. We showed that a mutant with reduced cholesterol content is more sensitive to fusion with Sendai virus than the parental cell with higher cholesterol content. Low cholesterol content in the cell membrane might cause modification of the lipid composition or membrane proteins, and these changes in the mutant cell membrane might induce enhanced fusion with viral envelope. Alternatively, cholesterol is required for fusion with viral envelope, but above a certain level it may inhibit fusion. Relevant somatic cell variants with altered response to fusion either with cells or/and with viruses have been isolated. Roos and his colleagues \[26-28\] have isolated somatic cell variants resistant to poly(ethylene glycol) (PEG), a potent fusion agent. The content membrane fatty acids in the resistant clone is different from that in the parental clone \[27\],a nd the variant shows an aberrant response to fusion with enveloped viruses (cited in Ref. 28). Toyama et al. also isolated mutants resistant to Sendai virus-induced cytolysis \[17\].T heir mutant showed a reduced response to fusion with cell membrane as well as fusion with viral envelope \[17,23\]:t he mutant was deficient in a sialyltransferase activity \[29\]T. hese studies with several variants suggest involvement of various cellular factors in the fusion processes. Further isolation of mutants with altered fusion steps could be a effective way to understand other cellular factor(s) necessary for fusion. We thank Dr. S. Yamada and Dr. K. Kawasaki (Kyoto University) for their fruitful discussion. This study is partly supported by a grant-in-aid for Cancer Research from the Ministry of Education, Science and Culture, Japan.",
year = "1987",
month = nov,
day = "2",
doi = "10.1016/0005-2736(87)90099-X",
language = "English",
volume = "904",
pages = "159--164",
journal = "BBA - Biomembranes",
issn = "0005-2736",
publisher = "Elsevier",
number = "1",
}