ArticleGenome biology2008
Identification of motifs that function in the splicing of non-canonical introns.
Article in Genome biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Computational meta-analysis of ribosomal RNA fragments: potential targets and interaction mechanisms.Nucleic acids research · 2021Pooled it
- Comprehensive analysis of the Kinetoplastea intron landscape reveals a novel intron-containing gene and the first exclusively trans-splicing eukaryote.BMC biology · 2024Article
- Development and validation of AI/ML derived splice-switching oligonucleotides.Molecular systems biology · 2024Article
- A single-cell strategy for the identification of intronic variants related to mis-splicing in pancreatic cancer.NAR genomics and bioinformatics · 2024Article
- A protein-encoding CCDC7 circular RNA inhibits the progression of prostate cancer by up-regulating FLRT3.NPJ precision oncology · 2024Article
- Statistical analysis of synonymous and stop codons in pseudo-random and real sequences as a function of GC content.Scientific reports · 2023Article
- Evolution of the Early Spliceosomal Complex-From Constitutive to Regulated Splicing.International journal of molecular sciences · 2021Review
- Genome-wide discovery of natural variation in pre-mRNA splicing and prioritising causal alternative splicing to salt stress response in rice.The New phytologist · 2021Article
- Wheat (Plants (Basel, Switzerland) · 2021Article
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- Inferring targeting modes of Argonaute-loaded tRNA fragments.RNA biology · 2020Article
- In Silico Analysis of a Highly Mutated Gene in Cancer Provides Insight into Abnormal mRNA Splicing: Splicing Factor 3B Subunit 1Biomolecules · 2020Article
- Characterizing the interplay between gene nucleotide composition bias and splicing.Genome biology · 2019Article
- In vivo Application of the REMOTE-control System for the Manipulation of Endogenous Gene Expression.Journal of visualized experiments : JoVE · 2019Article
- Mechanisms for U2AF to define 3' splice sites and regulate alternative splicing in the human genome.Nature structural & molecular biology · 2014Article
- YB-1 binds to CAUC motifs and stimulates exon inclusion by enhancing the recruitment of U2AF to weak polypyrimidine tracts.Nucleic acids research · 2012Article
- Frequent gain and loss of intronic splicing regulatory elements during the evolution of vertebrates.Genome biology and evolution · 2012Article
- Article
- Autoregulated splicing of muscleblind-like 1 (MBNL1) Pre-mRNA.The Journal of biological chemistry · 2011Article
- Allele-specific recognition of the 3' splice site of INS intron 1.Human genetics · 2010Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundWhile the current model of pre-mRNA splicing is based on the recognition of four canonical intronic motifs (5' splice site, branchpoint sequence, polypyrimidine (PY) tract and 3' splice site), it is becoming increasingly clear that splicing is regulated by both canonical and non-canonical splicing signals located in the RNA sequence of introns and exons that act to recruit the spliceosome and associated splicing factors. The diversity of human intronic sequences suggests the existence of novel recognition pathways for non-canonical introns. This study addresses the recognition and splicing of human introns that lack a canonical PY tract. The PY tract is a uridine-rich region at the 3' end of introns that acts as a binding site for U2AF65, a key factor in splicing machinery recruitment.
resultsHuman introns were classified computationally into low- and high-scoring PY tracts by scoring the likely U2AF65 binding site strength. Biochemical studies confirmed that low-scoring PY tracts are weak U2AF65 binding sites while high-scoring PY tracts are strong U2AF65 binding sites. A large population of human introns contains weak PY tracts. Computational analysis revealed many families of motifs, including C-rich and G-rich motifs, that are enriched upstream of weak PY tracts. In vivo splicing studies show that C-rich and G-rich motifs function as intronic splicing enhancers in a combinatorial manner to compensate for weak PY tracts.
conclusionThe enrichment of specific intronic splicing enhancers upstream of weak PY tracts suggests that a novel mechanism for intron recognition exists, which compensates for a weakened canonical pre-mRNA splicing motif.
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