ArticleMolecular and cellular biology1994
Control of transcription arrest in intron 1 of the murine adenosine deaminase gene.
Article in Molecular and cellular biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- Characterization of a novel RNA polymerase II arrest site which lacks a weak 3' RNA-DNA hybrid.Nucleic acids research · 2004Article
- Molecular events involved in up-regulating human Na+-independent neutral amino acid transporter LAT1 during T-cell activation.The Biochemical journal · 2001Article
- Transcriptional pause, arrest and termination sites for RNA polymerase II in mammalian N- and c-myc genes.Nucleic acids research · 1999Article
- Dissection of transcription factor TFIIF functional domains required for initiation and elongation.Proceedings of the National Academy of Sciences of the United States of America · 1995Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Transcription arrest plays a key role in the regulation of the murine adenosine deaminase (ADA) gene, as well as a number of other cellular and viral genes. We have previously characterized the ADA intron 1 arrest site, located 145 nucleotides downstream of the transcription start site, with respect to sequence and elongation factor requirements. Here, we show that the optimal conditions for both intron 1 arrest and overall ADA transcription involve the addition of high concentrations of KCl soon after initiation. As we have further delineated the sequence requirements for intron 1 arrest, we have found that sequences downstream of the arrest site are unnecessary for arrest. Also, a 24-bp fragment containing sequences upstream of the arrest site is sufficient to generate arrest downstream of the adenovirus major late promoter only in the native orientation. Surprisingly, we found that deletion of sequences encompassing the ADA transcription start site substantially reduced intron 1 arrest, with no effect on overall levels of transcription. At the same time, deletion of sequences upstream of the TATA box had no significant effect on either process. We believe the start site mutations have disrupted either the assembly or the composition of the transcription complex such that intron 1 site read-through is now favored. This finding, coupled with the increase in overall transcription after high-concentration KCl treatment, allows us to further refine our model of ADA gene regulation.
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