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Overexpression of actin in AcMNPV-infected cells interferes with polyhedrin synthesis and polyhedra formation

L Volkman1, K Storm, V Aivazachvili

  • 1Department of Plant and Microbial Biology, University of California, Berkeley 94720, USA. lvolkman@nature.berkeley.edu.

Virology
|November 15, 1996
PubMed

Insights

Autographa californica M nuclear polyhedrosis virus (AcMNPV) normally stops host protein synthesis. However, increased actin synthesis delays viral polyhedrin production and affects polyhedron formation.

Area of Science:

  • Virology
  • Molecular Biology
  • Insect Pathology

Background:

  • Autographa californica M nuclear polyhedrosis virus (AcMNPV) inhibits host protein synthesis late in infection.
  • Cytochalasin D treatment prolongs host actin synthesis and delays viral polyhedrin overexpression.

Purpose of the Study:

  • To investigate the causal relationship between actin synthesis and polyhedrin synthesis during AcMNPV infection.
  • To determine if elevated actin levels negatively impact viral polyhedrin production and polyhedron formation.

Main Methods:

  • Construction of recombinant viruses engineered to express actin at varying levels.
  • Analysis of polyhedrin synthesis and polyhedron formation in infected cells.

Main Results:

  • Expression of actin via a strong promoter significantly interfered with polyhedrin synthesis at a posttranscriptional level.
  • Increased actin expression also inhibited the formation of viral polyhedra.

Conclusions:

  • Actin synthesis negatively regulates viral polyhedrin production and polyhedron assembly.
  • This mechanism may explain the limited polyhedron formation observed in vivo.

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