Expression of polyoma early functions in mouse embryonal carcinoma cells depends on sequence rearrangements in the beginning of the late region.

Established mouse cell lines, primary cultures of mouse cells, and differentiated cell lines derived from mouse teratocarcinoma are permissive to polyoma virus. No viral early or late functions are expressed upon infection and penetration of multipotential embryonal cell lines. Polyoma mutants capable of growth on these cells were isolated and their DNA was cloned. Both the linear cloned viral DNA and a hybrid composed of mutant Bam HI (0.58) to Bgl I (0.72) 750 bp fragment (containing the origin of replication) ligated to the complementary wild-type 4.5 kb fragment are able to multiply on PCC4 embryonal carcinoma cells. The nucleotide sequence of two mutants indicated a genomic rearrangement on the late side of the origin, in which a deletion starting at nucleotides 46 (Py 204) and 77 (Py97) and terminating for both in nucleotide 107 was replaced by the duplication of a downstream late sequence starting at nucleotide 138 (Py 204) and 157 Py97) and terminating in nucleotide 220. The fact that the sequence rearrangements permit the expression of early and late functions upon infection suggests that this region participates in the control of early transcription. This control is different in embryonal and differentiated mouse cells.