The α promoter regulator-ovalbumin chimeric gene resident in human cells is regulated like the authentic α 4 gene after infection with herpes simplex virus 1 mutants in α 4 gene

Abstract

Human TK − 143 cells were converted to TK + phenotype with a plasmid containing the native herpes simplex virus 1 (HSV-1), thymidine kinase, a β gene, and a chimeric ovalbumin gene consisting of the coding sequences of the ovalbumin gene linked to the promoter-regulatory region of the HSV-1 α 4 gene. Comparison of the synthesis of ovalbumin and the α 4 gene product in the converted cells infected with ts mutants in α 4 gene and incubated at the permissive (33°C) and nonpermissive (39°C) temperatures revealed the following. (i) The synthesis of both ovalbumin and α 4 gene product was transiently induced at the permissive temperature but continued at elevated levels for many hours at the nonpermissive temperature. (ii) The synthesis of both ovalbumin and α 4 gene products resumed when the infected cells were shifted from permissive to nonpermissive temperature after the shut-off of α protein synthesis. (iii) Although both the β-TK and α 4-ovalbumin chimeric genes were covalently linked on the same plasmid, each was regulated independently. We conclude that α gene regulation is determined solely by (a) the inducer and (b) the induction sequence contained in the promoter-regulatory region and not by the location or the higher order structure of the immediate environment of the gene.