Mechanisms and Regulation of Alternative Pre-mRNA Splicing
Open accessAbstract
Precursor messenger RNA (pre-mRNA) splicing is a critical step in the posttranscriptional regulation of gene expression, providing significant expansion of the functional proteome of eukaryotic organisms with limited gene numbers. Split eukaryotic genes contain intervening sequences or introns disrupting protein-coding exons, and intron removal occurs by repeated assembly of a large and highly dynamic ribonucleoprotein complex termed the spliceosome, which is composed of five small nuclear ribonucleoprotein particles, U1, U2, U4/U6, and U5. Biochemical studies over the past 10 years have allowed the isolation as well as compositional, functional, and structural analysis of splicing complexes at distinct stages along the spliceosome cycle. The average human gene contains eight exons and seven introns, producing an average of three or more alternatively spliced mRNA isoforms. Recent high-throughput sequencing studies indicate that 100% of human genes produce at least two alternative mRNA isoforms. Mechanisms of alternative splicing include RNA–protein interactions of splicing factors with regulatory sites termed silencers or enhancers, RNA–RNA base-pairing interactions, or chromatin-based effects that can change or determine splicing patterns. Disease-causing mutations can often occur in splice sites near intron borders or in exonic or intronic RNA regulatory silencer or enhancer elements, as well as in genes that encode splicing factors. Together, these studies provide mechanistic insights into how spliceosome assembly, dynamics, and catalysis occur; how alternative splicing is regulated and evolves; and how splicing can be disrupted by cis- and trans-acting mutations leading to disease states. These findings make the spliceosome an attractive new target for small-molecule, antisense, and genome-editing therapeutic interventions.
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Alternative splicing patterns are regulated by specialized pre-mRNA binding proteins that alter spliceosome assembly at specific splice sites.
“Alternative splicing patterns (BOX 1) are regulated by specialized pre-mRNA binding proteins that alter spliceosome assembly at specific splice sites5–8”
From The neurogenetics of alternative splicing (2016) · cites this paper as [8]
U2 snRNA binds to the branch point during spliceosome assembly and then forms base pairs with U6 snRNA to become a key portion of the spliceosome catalytic centre for all major class introns.
“U2 snRNA binds to the branch point during spliceosome assembly and then forms base pairs with the U6 snRNA to become a key portion of the spliceosome catalytic centre for all major class introns6,8,183,184”
From The neurogenetics of alternative splicing (2016) · cites this paper as [8]
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An exonic splicing silencer represses spliceosome assembly after ATP-dependent exon recognition
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U1 snRNA Directly Interacts with Polypyrimidine Tract-Binding Protein during Splicing Repression
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CRYO-ELECTRON MICROSCOPY OF SPLICEOSOMAL COMPONENTS
Stark, H., & Lührmann, R. (2006) · Annual Review of Biophysics and Biomolecular Structure · doi:10.1146/annurev.biophys.35.040405.101953 · Cited by 97 · see citing works
Flagged first, then by citations
Research works printed but not linked: 1
- [253]Burge CB Tuschl T Sharp PA 1999 Splicing of Precurors to mRNAs by the Spliceosome Cold Spring Harbor, NY Cold Spring Harbor Lab. Press 525 60
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A large-scale binding and functional map of human RNA-binding proteins
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The neurogenetics of alternative splicing
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Structural basis of splicing modulation by antitumor macrolide compounds
Cretu, C., Agrawal, A. A., Cook, A., Will, C. L., Fekkes, P., Smith, P. G., Lührmann, R., Larsen, N., Buonamici, S., & Pena, V. (2018) · Molecular Cell · doi:10.1016/j.molcel.2018.03.011 · Cited by 174 · see citing works
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Gene expression is encoded in all parts of a co-evolving interacting gene regulatory structure
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The Glucocorticoid Receptor: Isoforms, Functions, and Contribution to Glucocorticoid Sensitivity
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Alternative splicing rewires Hippo signaling pathway in hepatocytes to promote liver regeneration
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Cardiac splicing as a diagnostic and therapeutic target
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- Authors
- Lee, Y., & Rio, D. C.
- Affiliations
- University of California, Berkeley (US)
- Corresponding author
- Rio, Donald C.
- Venue
- Annual Review of Biochemistry
- Publisher
- Annual Reviews
- Published
- 2015-06-02
- Volume
- 84
- Issue
- 1
- Pages
- 291-323
- ISSN
- 0066-4154 (ISSN-L)
- 1545-4509
- PMC
- PMC4526142
- OpenAlex
- W2153833484
- Cited by
- 1,291
- References
- 259
- Citations by year
- 2026: 82 · 2025: 105 · 2024: 139 · 2023: 142 · 2022: 162 · 2021: 153 · 2020: 127 · 2019: 117 · 2018: 97 · 2017: 90 · 2016: 53 · 2015: 22 · 2014: 1
- FWCI
- 8.47
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annual Review of Biochemistry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute of General Medical Sciences (R01GM097352, R01GM104385, P50GM102706, R01GM094890)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Research and Splicing
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA regulation and disease
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA and protein synthesis mechanisms
- Keywords
- alternative splicing, spliceosome, intron removal, RNA-protein interactions, RNA-RNA base pairing, splicing mutation, splicing factor mutations, antisense therapy, genome editing
- MeSH terms
- Animals, Disease, Gene Expression Regulation, Humans, Mutation, RNA Precursors, RNA Splicing, RNA, Catalytic, Spliceosomes, Alternative Splicing, Ribonucleoproteins, Small Nuclear
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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