ArticleNucleic acids research1994
A genetic polymorphism within the third poly(A) signal of the DHFR gene alters the polyadenylation pattern of DHFR transcripts in CHL cells.
Article in Nucleic acids research, 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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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Poly(A) signal-dependent degradation of unprocessed nascent transcripts accompanies poly(A) signal-dependent transcriptional pausing in vitro.RNA (New York, N.Y.) · 2010Article
- Analysis of circadian pattern reveals tissue-specific alternative transcription in leptin signaling pathway.BMC bioinformatics · 2007Article
- Repression of E2F1-mediated transcription by the ErbB3 binding protein Ebp1 involves histone deacetylases.Nucleic acids research · 2003Article
- Molecular cloning and characterization of chemokine-like factor 1 (CKLF1), a novel human cytokine with unique structure and potential chemotactic activity.The Biochemical journal · 2001Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
Two polymorphic dihydrofolate reductase (DHFR) alleles, termed 20 K and 21 K, exist in Chinese hamster lung cells. Three major transcripts of different lengths are transcribed from each allele, and the expression of these transcripts differs dramatically between the alleles as a result of differential utilization of three poly(A) sites. Transcripts from the 20 K allele are preferentially polyadenylated at the first poly(A) site, while those from the 21 K allele are preferentially polyadenylated at the third site. In this study, transient expression experiments were used to demonstrate that a 2.1 kb genomic fragment containing the three DHFR poly(A) sites is sufficient to reproduce the allele-specific polyadenylation pattern on transiently expressed CAT-DHFR transcripts in COS cells. Site-directed mutagenesis allowed identification of the sequence elements which are responsible for this allele-specific polyadenylation. These studies indicate that a single-base change in the third poly(A) signal sequence, which alters the consensus AAUAAA signal in the 21 K allele to a weak AAUAAU signal in the 20 K allele, is primarily responsible for the dramatic difference in polyadenylation between the two alleles. Thus, as a result of this single-base change in the third poly(A) signal sequence, utilization of the first poly(A) site, located 1.2 kb upstream, changes dramatically.
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