ArticleNature communications2020
Mutational bias and the protein code shape the evolution of splicing enhancers.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Alternative Splicing: A Critical Regulator in Human Bone Biology and Tumor Progression.Research (Washington, D.C.) · 2025Review
- Exonic splicing code and coordination of divalent metals in proteins.Nucleic acids research · 2024Article
- Purifying selection against spurious splicing signals contributes to the base composition evolution of the polypyrimidine tract.Journal of evolutionary biology · 2023Article
- A mutation-induced drug resistance database (MdrDB).Communications chemistry · 2023Article
- iEnhancer-ELM: improve enhancer identification by extracting position-related multiscale contextual information based on enhancer language models.Bioinformatics advances · 2023Article
- Selection of Olduvai Domains during Evolution: A Role for Primate-Specific Splicing Super-Enhancer and RNA Guanine Quadruplex in BipartiteBrain sciences · 2022Article
- Exonic splicing code and protein binding sites for calcium.Nucleic acids research · 2022Article
- Oligo Pools as an Affordable Source of Synthetic DNA for Cost-Effective Library Construction in Protein- and Metabolic Pathway Engineering.Chembiochem : a European journal of chemical biology · 2022Review
- Co-transcriptional splicing efficiency is a gene-specific feature that can be regulated by TGFβ.Communications biology · 2022Article
- How Sequence Context-Dependent Mutability Drives Mutation Rate Variation in the Genome.Genome biology and evolution · 2022Article
- Evidence in disease and non-disease contexts that nonsense mutations cause altered splicing via motif disruption.Nucleic acids research · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Exonic splicing enhancers (ESEs) are enriched in exons relative to introns and bind splicing activators. This study considers a fundamental question of co-evolution: How did ESE motifs become enriched in exons prior to the evolution of ESE recognition? We hypothesize that the high exon to intron motif ratios necessary for ESE function were created by mutational bias coupled with purifying selection on the protein code. These two forces retain certain coding motifs in exons while passively depleting them from introns. Through the use of simulations, genomic analyses, and high throughput splicing assays, we confirm the key predictions of this hypothesis, including an overlap between protein and splicing information in ESEs. We discuss the implications of mutational bias as an evolutionary driver in other cis-regulatory systems.
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Registered trials
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.