Abstract
Hyperexpression of polh and p10, two very late genes, is one of the remarkable characteristics in the baculovirus life cycle. However, the mechanisms underlying the hyperexpression of these two genes are still incompletely understood. In this study, actin was identified as a highly potential binding partner of polh and p10 promoters by conducting DNA pull-down and LC–MS/MS analyses. Inhibiting actin dynamics delayed and decreased the transcription of polh and p10. Actin interacted with viral RNA polymerase and transcription regulators, and the nuclear import of viral polymerase was inhibited with the disruption of actin dynamics. Simultaneously, the high enrichment of actin in polh and p10 promoters discovered via a chromatin immunoprecipitation (ChIP) assay indicated that actin was a component of the viral polymerase TIC. Moreover, overexpression of actin surprisingly upregulated the expression of luciferase (Luc) under the control of polh and p10 promoters. Taken together, actin participated in the hyperexpression of polh and p10 as a component of TIC. These results facilitate the promotion of the expression efficiency of foreign genes in the baculovirus expression vector system (BEVS).
Highlights
Baculoviruses are the enveloped, double-stranded DNA viruses, which primarily infect the lepidopteran insects
We discovered that actin played an important role in the hyperexpression of two very late genes, polh and p10
Actin has no inherent DNA-binding capability, but it is enriched in the polh and p10 promoters via promoter-binding partners
Summary
Baculoviruses are the enveloped, double-stranded (ds) DNA viruses, which primarily infect the lepidopteran insects They have been widely used as environmentally benign pesticides and recently developed for mammalian gene delivery [1]. One of the amazing phenomena in the baculovirus life cycle is the hyperexpression of two very late genes, polh and p10, resulting in the production of the occlusion body in which progeny virions are embedded. Both of these genes are not essential for viral replication and, thereby, can be deleted or replaced by foreign genes. It is of great necessity and significance to deeply elucidate the mechanism underlying the hyperexpression of these two very late genes
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