Title: Regulation of Junonia coenia Densovirus P9 Promoter Expression Authors
|Bossin, Herve - FAO/IAEA AUSTRIA, USDA|
|Gillett, Jennifer - ENT & NEM, UNIV OF FL|
Submitted to: Insect Molecular Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: June 27, 2007
Publication Date: August 22, 2007
Citation: Shirk, P.D., Bossin, H., Furlong, R.B., Gillett, J.L. 2007. Regulation of Junonia coenia Densovirus P9 Promoter Expression. Insect Molecular Biology. Interpretive Summary: The control of pest insects by conventional chemical strategies is in jeopardy due to the loss of most insecticides because of acquired resistance or environmental hazard. This has left the industry with fewer options for pest control. Scientists at the USDA ARS, Center from Medical, Agricultural and Veterinary Entomology have identified a region in the genome of an insect densovirus that controls the virus gene activity. Expression of these virus genes is dependent on a DNA sequence internal to the virus genome. The use of these genes as a transfer vector depends on the inclusion of this sequence in the development. Hence, this work favors the possibility of alternative methods of pest control.
Technical Abstract: Transcriptional activity of the Junonia coenia densovirus (JcDNV) P9 promoter depends on a 557 bp sequence located within the overlapping 3’ sequences for viral capsid and non-structural genes. Utilizing a somatic transformation assay to assess JcDNV activity in Drosophila melanogaster and Plodia interpunctella, viral sequences were subjected to deletional analysis. Removal of a 685 bp fragment reduced P9 driven expression to background. Inclusion of a second expression cassette demonstrated vector persistence and confirmed somatic transformation. P9 promoter driven expression was restored by insertion of a 557 bp JcDNV fragment or by inclusion of a heterologous baculovirus hr5 enhancer. Binding sites for PRE transcriptional factors were identified within the 557 bp fragment by comparison which suggests a potential role in regulating densoviral transcription.