Open AccessAlteration in phospholipid methylation and impairment of signal transmission in persistently paramyxovirus-infected C6 rat glioma cells.
Author(s) -
Peter A. Münzel,
Klaus Koschel
Publication year - 1982
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.79.12.3692
Subject(s) - phosphatidylethanolamine , measles virus , methylation , receptor , biology , virology , subacute sclerosing panencephalitis , virus , phospholipid , biochemistry , phosphatidylcholine , measles , gene , vaccination , membrane
The paramyxoviruses measles (subacute sclerosing panencephalitis, SSPE) virus and canine distemper virus (CDV) cause an impairment of the catecholamine-induced beta-adrenergic receptor-dependent cAMP generation in persistently infected C6 rat glioma cells. In C6 cells persistently infected with CDV the number of receptors is greatly reduced. Hirata and Axelrod have shown that the number of beta-adrenergic receptors could be regulated by methylation of phosphatidylethanolamine, resulting in lecithin synthesis [Hirata, F. & Axelrod, J. (1980) Science 209, 1082-1090]. We have therefore studied the methylation of phosphatidylethanolamine in persistently infected cells by the incorporation of [3H]methyl groups from [methyl-3H]methionine into phosphatidylethanolamine. In both infected systems, C6/ SSPE and C6/CDV, we observed a total loss of catecholamine-stimulated beta-adrenergic receptor-dependent methylation, whereas the beta-receptor-independent methylation of phospholipids was unchanged.