期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：1976
卷号：73
期号：11
页码：4022-4026
DOI：10.1073/pnas.73.11.4022
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Infection of primary cultures of mouse kidney cells with polyoma virus causes a biphasic increase in the activities of L-ornithine decarboxylase (ODC; L-ornithine carboxy-lyase; EC 4.1.1.17 ) and S-adenosyl-L-methionine decarboxylase (SAMD; S-adenoxyl-L-methionine carboxy-lyase; EC 4.1.50), as well as in the level of the polyamines putrescine, spermidine, and spermine. An early peak occurs during the period when early viral mRNA is synthesized and prior to the onset of virus-induced synthesis of host cell DNA. A late peak coincides in time with the maximum rate of virus-induced synthesis of cellular DNA. A similar biphasic stimulation of polyamine synthesis is induced even when DNA synthesis is prevented by 5-fluorodeoxyuridine. Actinomycin D (AMD) in a dose that inhibits rRNA synthesis causes no inhibition of ODC or SAMD. In a dose that inhibits mRNA synthesis as well, short-term AMD treatment causes "superinduction" of ODC but inhibition of SAMD. Prolonged treatment with the high dose of AMD inhibits ODC as well, indicating that late ODC activity may be dependent on mRNA synthesized during early infection. Cycloheximide effectively obliterates the ODC and SAMD activities during the entire infectious cycle. Uncoupling from DNA and rRNA synthesis suggests that polyamine synthesis is regulated independently of these events. The experiments with AMD and cycloheximide suggest that the formation of ODC is subject to post-transcriptional control, whereas that of SAMD is regulated primarily at the transcriptional level.
