ArticleGenome biology and evolution2013
Distinct mutational behaviors differentiate short tandem repeats from microsatellites in the human genome.
Article in Genome biology and evolution, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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43 citing papers in PubMed, 68 citations in OpenAlex.
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- Application of PCR-HRM method for microsatellite polymorphism genotyping in the LDHA gene of pigeons (Columba livia).PloS one · 2021Article
- Finding and extending ancient simple sequence repeat-derived regions in the human genome.Mobile DNA · 2020Article
- The Impact of Natural Selection on Short Insertion and Deletion Variation in the Great Tit Genome.Genome biology and evolution · 2019Article
- Microsatellite Stability in STR AnalysisFrontiers in cellular and infection microbiology · 2019Article
- New Methods for Inferring the Distribution of Fitness Effects for INDELs and SNPs.Molecular biology and evolution · 2018Article
- The effects of transcription and recombination on mutational dynamics of short tandem repeats.Nucleic acids research · 2018Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
A tandem repeat's (TR) propensity to mutate increases with repeat number, and can become very pronounced beyond a critical boundary, transforming it into a microsatellite (MS). However, a clear understanding of the mutational behavior of different TR classes and motifs and related mechanisms is lacking, as is a consensus on the existence of a boundary separating short TRs (STRs) from MSs. This hinders our understanding of MSs' mutational properties and their effective use as genetic markers. Using indel calls for 179 individuals from 1000 Genomes Pilot-1 Project, we determined polymorphism incidence for four major TR classes, and formalized its varying relationship with repeat number using segmented regression. We observed a biphasic regime with a transition from a faster to a slower exponential growth at 9, 5, 4, and 4 repeats for mono-, di-, tri-, and tetranucleotide TRs, respectively. We used an in vitro mutagenesis assay to evaluate the contribution of strand slippage errors to mutability. STRs and MSs differ in their absolute polymorphism levels, but more importantly in their rates of mutability growth. Although strand slippage is a major factor driving mononucleotide polymorphism incidence, dinucleotide polymorphism incidence is greater than that expected due to strand slippage alone, indicating that additional cellular factors might be driving dinucleotide mutability in the human genome. Leveraging on hundreds of human genomes, we present the first comprehensive, genome-wide analysis of TR mutational behavior, encompassing several motif sizes and compositions.
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