ArticleRNA (New York, N.Y.)1999
The role of overlapping U1 and U11 5' splice site sequences in a negative regulator of splicing.
Article in RNA (New York, N.Y.), 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- Fully haplotyped genome assemblies of healthy individuals reveal variability in 5'ss strength and support by splicing regulatory proteins.NAR genomics and bioinformatics · 2025Article
- Retroviral RNA Processing.Viruses · 2022Review
- At the Intersection of Major and Minor Spliceosomes: Crosstalk Mechanisms and Their Impact on Gene Expression.Frontiers in genetics · 2021Review
- Evidence that a threshold of serine/arginine-rich (SR) proteins recruits CFIm to promote rous sarcoma virus mRNA 3' end formation.Virology · 2016Article
- HnRNPH1/H2, U1 snRNP, and U11 snRNP cooperate to regulate the stability of the U11-48K pre-mRNA.RNA (New York, N.Y.) · 2013Article
- Juxtaposition of two distant, serine-arginine-rich protein-binding elements is required for optimal polyadenylation in Rous sarcoma virus.Journal of virology · 2011Article
- Structural and functional analysis of the Rous Sarcoma virus negative regulator of splicing and demonstration of its activation by the 9G8 SR protein.Nucleic acids research · 2011Article
- Article
- RNA processing control in avian retroviruses.Frontiers in bioscience : a journal and virtual library · 2008Review
- Serine/arginine-rich proteins contribute to negative regulator of splicing element-stimulated polyadenylation in rous sarcoma virus.Journal of virology · 2007Article
- The negative regulator of splicing element of Rous sarcoma virus promotes polyadenylation.Journal of virology · 2006Article
- The retrovirus RNA trafficking granule: from birth to maturity.Retrovirology · 2006Review
- Retroviral splicing suppressor sequesters a 3' splice site in a 50S aberrant splicing complex.Molecular and cellular biology · 2005Article
- Solution structure of the pseudo-5' splice site of a retroviral splicing suppressor.RNA (New York, N.Y.) · 2004Article
- Packaging and reverse transcription of snRNAs by retroviruses may generate pseudogenes.RNA (New York, N.Y.) · 2004Article
- A novel approach to describe a U1 snRNA binding site.Nucleic acids research · 2003Article
- Silent point mutation in an avian retrovirus RNA processing element promotes c-myb-associated short-latency lymphomas.Journal of virology · 2003Article
- SRp30c is a repressor of 3' splice site utilization.Molecular and cellular biology · 2002Article
- Efficient polyadenylation of Rous sarcoma virus RNA requires the negative regulator of splicing element.Nucleic acids research · 2002Article
- Retroviral splicing suppressor requires three nonconsensus uridines in a 5' splice site-like sequence.Journal of virology · 2001Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Splicing of Rous sarcoma virus RNA is regulated in part by a cis-acting intronic RNA element called the negative regulator of splicing (NRS). An NRS mutant affecting nt 916-923 disrupts U11 snRNP binding and reduces NRS activity (Gontarek et al., 1993, Genes & Dev 7:1926-1936). However, we observed that a U15' splice site-like sequence, which overlapped the U11 site, was also disrupted by this mutation. To determine whether the U1 or the U11 site was essential for NRS activity, we analyzed twelve additional mutants involving nt 915-926. All mutations that disrupted the potential base pairing between U1 snRNA and the NRS reduced NRS activity, including single point mutations at nt 915, 916, and 919. The point mutation at nt 919 was partially suppressed by a compensatory base change mutation in U1 snRNA. In contrast, a mutation which strengthened the potential base pairing between the U1 site and the NRS increased NRS activity. Surprisingly, mutations that specifically targeted the U115' splice site consensus sequence increased the levels of unspliced RNA, suggesting U11 binding plays an antagonistic role to NRS activity. We propose that U1 snRNP binding to the NRS inhibits splicing and is regulated by U11 snRNP binding to the overlapping sequence. Competition between U1 and U11 snRNPs would result in the appropriate balance of spliced to unspliced RNAs for optimal viral replication. Further, a virus mutated in the U1/U11 region of the NRS was found to have delayed replication.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.