A single-base deletion within the protein-coding region of the adenovirus type 5 early region lA (EIA) genes, 399 bases downstream from the transcription start site, depresses transcription to 2% of the wild-type rate. Complementation studies demonstrated that this was due to two effects of the mutation: first, inactivation of an ElA protein, causing a reduction by a factor of 5; second, a defect which acts in cis to depress EIA mRNA and nuclear RNA concentrations by a factor of 10. A larger deletion within the protein-coding region of ElA which overlaps the single-base deletion produces the same phenotype. In contrast, a linker insertion which results in a similar truncated EIA protein does not produce the cis-acting defect in EIA transcription. These results demonstrate that a critical cis-acting transcription control region occurs within the protein coding sequence in adenovirus type 5 ElA. The single-base deletion occurs in a sequence which shows extensive homology with a sequence from the enhancer regions of simian virus 40 and polyomavirus. This region is not required for ElA transcription during the late phase of infection.In Escherichia coli, promoter mutations generally result from changes in bases which interact directly with RNA polymerase and occur within 40 bases of the transcription initiation site (62, 68). In contrast to E. coli promoters, the DNA sequences which regulate the transcription of eucaryotic protein-coding genes, which are transcribed by RNA polymerase II, are more complex. The most highly conserved sequence element of polymerase II promoters, the TATA box (11; M. Goldberg, Ph.D. thesis, Stanford University, Stanford, Calif., 1978), centered about 27 bases upstream from the transcription start site, probably interacts directly with the polymerase. Deletion of this sequence usually leads to a reduction in the rate of transcription initiation by a factor of 5 to 10, and the residual transcripts usually have heterogeneous cap sites (18,25,32,34,49,56), which are sites of transcription initiation (15,36). Transcription initiation in vitro in most instances is completely dependent on the TATA sequence (16,40,59,72,78). However, in eucaryotic cells, mutations at much greater distances from the start site than are the TATA box or the -35 region of E. coli promoters can have profound effects on transcription initiation (5, 18, 21, 33-35, 49, 50, 53, 71). Several strong viral promoter regions contain sequences called enhancers, which can increase transcription from a variety of promoters by an unknown mechanism which is largely independent of their position relative to the transcription start site (4,17,21,22,44,45,52,75). Since the function of these more distant transcription control signals is largely independent of their distance from the transcription initiation site, it seems unlikely that they interact directly with RNA polymerase II (44,48,52).In most genes transcribed by RNA polymerase II which have been analyzed, DNA sequences required for transcription initiation lie upstream from th...
A single-base deletion within the protein-coding region of the adenovirus type 5 early region 1A (E1A) genes, 399 bases downstream from the transcription start site, depresses transcription to 2% of the wild-type rate. Complementation studies demonstrated that this was due to two effects of the mutation: first, inactivation of an E1A protein, causing a reduction by a factor of 5; second, a defect which acts in cis to depress E1A mRNA and nuclear RNA concentrations by a factor of 10. A larger deletion within the protein-coding region of E1A which overlaps the single-base deletion produces the same phenotype. In contrast, a linker insertion which results in a similar truncated E1A protein does not produce the cis-acting defect in E1A transcription. These results demonstrate that a critical cis-acting transcription control region occurs within the protein coding sequence in adenovirus type 5 E1A. The single-base deletion occurs in a sequence which shows extensive homology with a sequence from the enhancer regions of simian virus 40 and polyomavirus. This region is not required for E1A transcription during the late phase of infection.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.