Abstract
Previous studies have shown that herpes simplex virus genes form 3 groups, .alpha., .beta. and .gamma., whose expression is coordinately regulated and sequentially ordered in a cascade fashion. Chimeric genes constructed by fusion of the coding and 5'' nontranslated leader sequences of the thymidine kinase (TK) gene to the sequences upstream from the site of initiation of transcription of .alpha. genes 4 and 27 are regulated as .alpha. genes and are induced in mouse L cells converted to TK+ phenotype by infection with TK- virus. In .alpha. gne 4, both the promoter and the regulatory region are separable and movable. The promoter permits expression but not induction when fused to TK in the noncoding leader region of the gene. The regulator, when fused to the promoter of an expressible but noninducible portion of the natural .beta. TK, renders the gene inducible as an .alpha. gene; it consists of multiple regulatory units acting cumulatively. The precise site of initiation of transcription of .alpha. gene 0 within the inverted b sequences of the L component of viral DNA is reported. The following was also reported. The chimeric gene consisting of the coding and 5'' nontranslated leader regions of the TK gene fused to portions of the domain of .alpha. gene 0 extending largely upstream from the site of initiation of transcription of .alpha. gene 0 was regulated in the same fashion as the .alpha. 4- and .alpha. 27-TK chimeras. The regulatory region in the .alpha. gene 0 is largely upstream from nucleotide -140. The promoter-regulatory regions of .alpha. genes 0, 4 and 27 share TATA sequences, A + T-rich (consensus) sequences occurring in regulating regions of .alpha. gnes 0 and 4 in > 1 copy, and multiple G + C-rich inverted repeats. The relation of these sequences to the function of the promoter-regulatory regions of the .alpha. genes is discussed.