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Autoregulation of simian virus-40 gene-a by t-antigen

Academic Article
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Overview

authors

  • Reed, Steven
  • Stark, G. R.
  • Alwine, J. C.

publication date

  • 1976

journal

  • Proceedings of the National Academy of Sciences of the United States of America  Journal

abstract

  • 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.

subject areas

  • Antigens, Viral
  • Cell Line
  • Cell Nucleus
  • Cytoplasm
  • DNA, Viral
  • Genes
  • Kinetics
  • Mutation
  • RNA, Messenger
  • RNA, Viral
  • Simian virus 40
  • Temperature
  • Transcription, Genetic
  • Viral Proteins
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Identity

International Standard Serial Number (ISSN)

  • 0027-8424

Digital Object Identifier (DOI)

  • 10.1073/pnas.73.9.3083

PubMed ID

  • 184459
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Additional Document Info

start page

  • 3083

end page

  • 3087

volume

  • 73

issue

  • 9

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