ArticleNucleic acids research2013
Exon-phase symmetry and intrinsic structural disorder promote modular evolution in the human genome.
Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Review
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- Evolutionary and Regulatory Pattern Analysis of Soybean CaFrontiers in plant science · 2022Article
- 'Why genes in pieces?'-revisited.Nucleic acids research · 2019Article
- mRNA processing in mutant zebrafish lines generated by chemical and CRISPR-mediated mutagenesis produces unexpected transcripts that escape nonsense-mediated decay.PLoS genetics · 2017Article
- Three reasons protein disorder analysis makes more sense in the light of collagen.Protein science : a publication of the Protein Society · 2016Article
- Redefining the BH3 Death Domain as a 'Short Linear Motif'.Trends in biochemical sciences · 2015Review
- Splice junctions are constrained by protein disorder.Nucleic acids research · 2015Article
- Computer analysis of protein functional sites projection on exon structure of genes in Metazoa.BMC genomics · 2015Article
- The RIDL hypothesis: transposable elements as functional domains of long noncoding RNAs.RNA (New York, N.Y.) · 2014Article
- Sequence complexity of amyloidogenic regions in intrinsically disordered human proteins.PloS one · 2014Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A key signature of module exchange in the genome is phase symmetry of exons, suggestive of exon shuffling events that occurred without disrupting translation reading frame. At the protein level, intrinsic structural disorder may be another key element because disordered regions often serve as functional elements that can be effectively integrated into a protein structure. Therefore, we asked whether exon-phase symmetry in the human genome and structural disorder in the human proteome are connected, signalling such evolutionary mechanisms in the assembly of multi-exon genes. We found an elevated level of structural disorder of regions encoded by symmetric exons and a preferred symmetry of exons encoding for mostly disordered regions (>70% predicted disorder). Alternatively spliced symmetric exons tend to correspond to the most disordered regions. The genes of mostly disordered proteins (>70% predicted disorder) tend to be assembled from symmetric exons, which often arise by internal tandem duplications. Preponderance of certain types of short motifs (e.g. SH3-binding motif) and domains (e.g. high-mobility group domains) suggests that certain disordered modules have been particularly effective in exon-shuffling events. Our observations suggest that structural disorder has facilitated modular assembly of complex genes in evolution of the human genome.
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