Transcription and replication result in distinct epigenetic marks following repression of early gene expression.

Simian virus 40 (SV40) early transcription is repressed when the product of early transcription, T-antigen, binds to its cognate regulatory sequence, Site I, in the promoter of the SV40 minichromosome. Because SV40 minichromosomes undergo replication and transcription potentially repression could occur during active transcription or during DNA replication. Since repression is frequently epigenetically marked by the introduction of specific forms of methylated histone H3, we characterized the methylation of H3 tails during transcription and replication in wild-type SV40 minichromosomes and mutant minichromosomes which did not repress T-antigen expression.

Virion-mediated transfer of SV40 epigenetic information.

In eukaryotes, epigenetic information can be encoded in parental cells through modification of histones and subsequently passed on to daughter cells in a process known as transgenerational epigenetic regulation. Simian Virus 40 (SV40) is a well-characterized virus whose small circular DNA genome is organized into chromatin and, as a consequence, undergoes many of the same biological processes observed in cellular chromatin. In order to determine whether SV40 is capable of transgenerational epigenetic regulation, we have analyzed SV40 chromatin from minichromosomes and virions for the presence of modified histones using various ChIP techniques and correlated these modifications with specific biological effects on the SV40 life cycle.

Histone H4 lysine 20 mono- and tri-methylation define distinct biological processes in SV40 minichromosomes.

The methylation profile of histone h4 on lysine 20 in sV40 chromatin during an infection was investigated using ChIp analyses with antibodies to monomethyl (h4K20me1), dimethyl (h4K20me2), and trimethyl (h4K20me3) histone h4. h4K20me1 was found in late-transcribing, uncoating, encapsidating and replicating minichromosomes as well as in the sV40 chromatin present in virions. Its prevalence was greatest in virions and least in minichromosomes present between 4 and 24 hours post-infection.