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Polyomavirus ALTOs, but not MTs, downregulate viral early gene expression by activating the NF-KB pathway

ABSTRACT: Polyomaviruses are small, circular dsDNA viruses that can cause cancer. Alternative splicing of polyomavirus early transcripts generates large and small tumor antigens (LT, ST) that play essential roles in viral replication and tumorigenesis. Some polyomaviruses also express middle tumor antigens (MTs) or alternate LT open reading frames (ALTOs), which are evolutionarily related but have distinct gene structures. MTs are a splice variant of the early transcript whereas ALTOs are overprinted on the second exon of the LT transcript in an alternate reading frame and are translated via an alternative start codon. Merkel cell polyomavirus (MCPyV), the only human polyomavirus that causes cancer, encodes an ALTO but its role in the viral lifecycle and tumorigenesis has remained elusive. In this MassIVE entry, we provide mass spectrometry data and result files associated with a TurboID experiment to identify human and viral proteins that bind to ALTO.

INSTRUMENT(S): Orbitrap eclipse w/FAIMS

ORGANISM(S): Merkel Cell Polyomavirus (ncbitaxon:493803) Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Denise Galloway

PROVIDER: MSV000095457 | MassIVE | Fri Jul 26 14:19:00 BST 2024

REPOSITORIES: MassIVE

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Polyomavirus ALTOs, but not MTs, downregulate viral early gene expression by activating the NF-κB pathway

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Hepatic gene expression in transgenic mice with conditional liver-specific expression of the SV40 17kT/LT oncoproteins

Project description:The SV40 large (LT) and small (st) antigens are produced from a single alternatively spliced pre-mRNA, that when co-expressed, transform a variety of cells in vitro and in vivo. However, 17kT, a relatively uncharacterized third protein that is co-linear with LT for the first 131 amino acids, is also produced from the early viral pre-mRNA by removal of an additional intron from the LT transcript. Here we report a line of transgenic mice expressing a liver-specific dox-inducible viral transcript that fails to yield any detectable LT protein, yet produces abundant 17kT. Comparative analysis of livers of transgenic mice expressing either 17kT or LT demonstrates that while 17kT is a potent stimulator of cell proliferation, it is ineffective at inducing liver tumor development, due in part, to the failure of 17kT to effectively induce the expression of growth regulators and reactivate expression of imprinted and developmentally regulated hepatic genes. These studies highlight key functional differences between LT and 17kT in their ability to transform quiescent primary epithelial cells in vivo, and demonstrate how specific functional domains within LT impact cell-specific gene expression to promote oncogenesis. Keywords: genetic modification, SV40, 17kT, LT, Rb, p53, hepatocellular carcinoma, hepatic hyperplasia, differentiation. Affymetrix mouse genome 430 A and B platform was used, single measurements for wild-type and transgenic animals.

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