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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Autoregulation of simian virus 40 gene A by T antigen.

During lytic infection by simian virus 40, gene A is transcribed into early RNA, which is translated into A protein (T antigen). Both the rate of synthesis and the intracellular amount of early RNA are higher in cells infected by temperature-sensitive A (tsA) mutants than in cells infected by wild-type virus. These differences are observed at permissive temperature (32 degrees) and are amplified greatly after a shift to restrictive temperature (41 degrees). For example, at 32 degrees cells infected by tsA mutants synthesize early RNA approximately twice as fast as cells infected by wild-type virus. After the shift to 41 degrees, the rate of synthesis in the tsA infection increases to 15 times the rate in the wild-type infection. In contrast, cells infected by tsA mutants do not overproduce late RNA. We suggest that the A protein regulates its own synthesis by negative feedback control of gene A transcription.[1]


  1. Autoregulation of simian virus 40 gene A by T antigen. Reed, S.I., Stark, G.R., Alwine, J.C. Proc. Natl. Acad. Sci. U.S.A. (1976) [Pubmed]
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