Earlier studies have shown that late, .gamma.2, genes of herpes simplex virus 1 stably incorporated into the environment of the cell are regulated as .beta. genes. For example, the induction of the intact gene specifying glycoprotein C (gC) resident in a clonal L cell line superinfected with a gC- virus was enhanced in the presence of inhibitory concentrations of phosphonoacetate (PAA), a viral DNA synthesis inhibitor. Moreover, the gene was induced by superinfection at the nonpermissive temperature with tsHA1, a temperature-sensitive (ts) DNA- virus mutant. In the viral genome, the gC gene is not expressed by the tsHA1 mutant at the nonpermissive temperature or by the mutant or wild-type virus at the permissive temperature in the presence of inhibitory concentrations of PAA. We report that expression of a truncated gC gene introduced in the same fashion and resident in a clonal L cell line was at least partially sensitive to PAA and was not induced by tsHA1 at the nonpermissive temperature. The gene was transcribed from a prokaryotic transcription initiation site in the plasmid. Induction of gene expression by superinfecting virus did not result in appreciable amplification of the gene. We conclude that gC, a .gamma.2 gene, contains two regulatory domains. The gene domain upstream from nucleotide +22 confers .beta.-like regulation, whereas the gene domain downstream from +22 confers .gamma.2 regulation. In the gene resident in cells in culture the upstream regulatory domain is dominant, whereas the converse is true for the gene resident in the viral genome.