The distal transcription signals of the herpesvirus tk gene share a common hexanucleotide control sequence.
The two distal transcription signals of the herpesvirus tk gene share a common hexanucleotide sequence and function in a mutually dependent manner. We examined their roles by introducing corresponding base mutations into each hexanucleotide. The effects of mutations in the hexanucleotide of the first distal signal match the pattern of effects of the corresponding mutations in the second distal signal. These concordant patterns suggest that the hexanucleotide repeats are functionally analogous. There is one difference between the two distal signals. Disruption of the second distal signal concomitantly inactivates the first distal signal; disruption of the first distal signal leads to only partial inactivation of the second distal signal. When the positions of the two distal signals are switched, the partial dependence of the second distal signal is alleviated. We suggest a model for positive transcriptional control analogous to activation of the cl maintenance promoter of bacteriophage lambda by repressor.
D000483:Alleles; D000818:Animals; D010582:Bacteriophage lambda / Q000235:genetics; D001483:Base Sequence; D005260:Female; D006564:Herpesviridae / Q000201:enzymology / Q000235:genetics*; D009154:Mutation; D009841:Oligonucleotides / Q000235:genetics; D009865:Oocytes / Q000378:metabolism; D009876:Operon; D010957:Plasmids; D013937:Thymidine Kinase / Q000235:genetics*; D014158:Transcription, Genetic; D014981:Xenopus
D009841:Oligonucleotides; D013937:Thymidine Kinase