ArticleMolecular and cellular biology1999
Assembly of the cleavage and polyadenylation apparatus requires about 10 seconds in vivo and is faster for strong than for weak poly(A) sites.
Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Enzymatically amplified linear dbDNAGene therapy · 2023Article
- Enhancers regulate 3' end processing activity to control expression of alternative 3'UTR isoforms.Nature communications · 2022Article
- A missense mutation in the CSTF2 gene that impairs the function of the RNA recognition motif and causes defects in 3' end processing is associated with intellectual disability in humans.Nucleic acids research · 2020Article
- Plant 3' Regulatory Regions From mRNA-Encoding Genes and Their Uses to Modulate Expression.Frontiers in plant science · 2020Review
- Article
- The Nrd1-like protein Seb1 coordinates cotranscriptional 3' end processing and polyadenylation site selection.Genes & development · 2016Article
- Temporal Dissection of Rate Limiting Transcriptional Events Using Pol II ChIP and RNA Analysis of Adrenergic Stress Gene Activation.PloS one · 2015Article
- Construction of a recombinant human insulin expression vector for mammary gland-specific expression in buffalo (Bubalus bubalis) mammary epithelial cell line.Molecular biology reports · 2014Article
- Transcript processing and export kinetics are rate-limiting steps in expressing vertebrate segmentation clock genes.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- A viral genome landscape of RNA polyadenylation from KSHV latent to lytic infection.PLoS pathogens · 2013Article
- A cytoplasmic negative regulator isoform of ATF7 impairs ATF7 and ATF2 phosphorylation and transcriptional activity.PloS one · 2011Article
- Molecular mechanisms of eukaryotic pre-mRNA 3' end processing regulation.Nucleic acids research · 2010Review
- Poly(A) signal-dependent degradation of unprocessed nascent transcripts accompanies poly(A) signal-dependent transcriptional pausing in vitro.RNA (New York, N.Y.) · 2010Article
- Gene regulation by sense-antisense overlap of polyadenylation signals.RNA (New York, N.Y.) · 2009Article
- Regulation of the steroidogenic acute regulatory protein gene expression: present and future perspectives.Molecular human reproduction · 2009Review
- Polyadenylation releases mRNA from RNA polymerase II in a process that is licensed by splicing.RNA (New York, N.Y.) · 2009Article
- A family of splice variants of CstF-64 expressed in vertebrate nervous systems.BMC molecular biology · 2009Article
- Structure of the yeast SR protein Npl3 and Interaction with mRNA 3'-end processing signals.Journal of molecular biology · 2008Article
- Functional coupling of last-intron splicing and 3'-end processing to transcription in vitro: the poly(A) signal couples to splicing before committing to cleavage.Molecular and cellular biology · 2008Article
- Recognition of GU-rich polyadenylation regulatory elements by human CstF-64 protein.The EMBO journal · 2003Article
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5 authors.
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Abstract
We have devised a cis-antisense rescue assay of cleavage and polyadenylation to determine how long it takes the simian virus 40 (SV40) early poly(A) signal to commit itself to processing in vivo. An inverted copy of the poly(A) signal placed immediately downstream of the authentic one inhibited processing by means of sense-antisense duplex formation in the RNA. The antisense inhibition was gradually relieved when the inverted signal was moved increasing distances downstream, presumably because cleavage and polyadenylation occur before the polymerase reaches the antisense sequence. Antisense inhibition was unaffected when the inverted signal was moved upstream. Based on the known rate of transcription, we estimate that the cleavage-polyadenylation process takes between 10 and 20 s for the SV40 early poly(A) site to complete in vivo. Relief from inhibition occurred earlier for shorter antisense sequences than for longer ones. This indicates that a brief period of assembly is sufficient for the poly(A) signal to shield itself from a short (50- to 70-nucleotide) antisense sequence but that more assembly time is required for the signal to become immune to the longer ones (approximately 200 nucleotides). The simplest explanation for this target size effect is that the assembly process progressively sequesters more and more of the RNA surrounding the poly(A) signal up to a maximum of about 200 nucleotides, which we infer to be the domain of the mature apparatus. We compared strong and weak poly(A) sites. The SV40 late poly(A) site, one of the strongest, assembles several times faster than the weaker SV40 early or synthetic poly(A) site.
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