| pubmed-article:8824775 | pubmed:abstractText | The genome of polyomaviruses is divided into two coding regions: the early and the late region. A relatively short regulatory sequence, encompassing the origin of viral DNA replication (ori), separates the two regions encoding the structural genes. In mouse polyomavirus (Py) in particular, the early DNA codes for three antigens: large, middle and small T-antigen (L-T, M-T and S-T, respectively). Large T antigen binds ori and thus regulates both viral DNA transcription and replication. Middle T antigen has been shown to mediate malignant transformation in non-permissive cells in vitro. No defined function has been assigned to the small T antigen although this gene product is thought to act synergistically both with L- and M-T antigens. The viral late region of Py encodes also three different genes whose products form the viral capsid during the productive infection cycle in permissive cells. Py early region was thought to be the only part of the genome necessary to code for proteins of functional and regulatory significance. The viral late region, on the other hand, was for a long time considered a simple reservoir of structural information, since it codes for capsid proteins and was supposedly devoid of functional control properties. This short review is focused on recent works from our and other laboratories, reporting evidence that in Py also the late region has a functional role since late sequences are involved in the control of viral DNA replication and in capsid assembly. Results indicating that this might be true for the cognate simian virus SV40 will be also reviewed. | lld:pubmed |
