Virus Name | Simian Virus 40 |
Virus Short Name | SV40 |
Order | Unassigned |
Virus Family | Polyomaviridae |
Virus Subfamily | N.A. |
Genus | Betapolyomavirus |
Species | Simian virus 40 |
Host | Mammals, human |
Cell Tropism | N.A. |
Associated Disease | N.A. |
Mode of Transmission | N.A. |
VIPR DB link | N.A. |
ICTV DB link | https://talk.ictvonline.org/ictv-reports/ictv_9th_report/dsdna-viruses-2011/w/dsdna_viruses/129/polyomaviridae |
Virus Host DB link | N.A. |
Paper Title | PP2A-dependent disruption of centrosome replication and cytoskeleton organization in Drosophila by SV40 small tumor antigen |
Author's Name | S Kotadia, LR Kao, SA Comerford, RT Jones, RE Hammer and TL Megraw |
Journal Name | Oncogene |
Pubmed ID | 18663356 |
Abstract | Viruses of the DNA tumor virus family share the ability to transform vertebrate cells through the action of virus-encoded tumor antigens that interfere with normal cell physiology. They accomplish this very efficiently by inhibiting endogenous tumor suppressor proteins that control cell proliferation and apoptosis. Simian virus 40 (SV40) encodes two oncoproteins, large tumor antigen, which directly inhibits the tumor suppressors p53 and Rb, and small tumor antigen (ST), which interferes with serine/threonine protein phosphatase 2A (PP2A). We have constructed a Drosophila model for SV40 ST expression and show that ST induces supernumerary centrosomes, an activity we also demonstrate in human cells. In early Drosophila embryos, ST also caused increased microtubule stability, chromosome segregation errors, defective assembly of actin into cleavage furrows, cleavage failure, a rise in cyclin E levels and embryonic lethality. Using ST mutants and genetic interaction experiments between ST and PP2A subunit mutations, we show that all of these phenotypes are dependent on STs interaction with PP2A. These analyses demonstrate the validity and utility of Drosophila as a model for viral oncoprotein function in vivo. |
Used Model | U2OS cells |
DOI | 10.1038/onc.2008.254 |