Abstract
Polyhedrin and p10, two proteins encoded by Autographa californica M nuclear polyhedrosis virus, are hyperexpressed very late during normal infections. In this study we found that cytochalasin D, a drug that leads to increased actin synthesis in infected and uninfected host cells, delayed the amplified expression of polyhedrin and p10 when added to infected cells before hyperexpression was already in progress. Restoration of polyhedrin and p10 hyperexpression could be achieved by removal of the drug, but required new protein synthesis. An inverse correlation was observed between polyhedrin/p10 mRNA levels and actin mRNA levels at late and very late times during infection, regardless of whether cytochalasin D was added, removed, or never present. In comparison to mRNAs of polyhedrin and p10 the mRNA levels of the early/late viral gene 39K were much less affected by cytochalasin D and responded to drug removal more slowly. The results of these studies revealed an apparent correlation between the shut down of host actin genes and the amplified expression of polyhedrin and p10 in the presence and absence of cytochalasin D. The possibility that newly synthesized actin itself, either directly or indirectly, plays a negative regulatory role in the accumulation of polyhedrin and p10 mRNAs is discussed.
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