GeneticsEvolutionary BiologyPeer-reviewed journal article
The selective dynamics of interruptions at short tandem repeats
Michael E. GoldbergiD, Harriet DashnowiD, Kelley HarrisiD, Aaron R. QuinlaniD
Abstract
Short tandem repeats (STRs) are hotspots of genomic instability that mutate at rates orders of magnitude greater than non-repetitive loci due to frequent replication slippage. Expansions at some STR loci cause Mendelian diseases, while variation at other noncoding loci may affect complex traits, possibly by altering transcription factor occupancy of nearby binding sites. Accordingly, some STRs are inferred to be under purifying selection, regardless of their instability. One or more "interruptions", or bases that disrupt the locuss canonical repeat, significantly decrease an STRs mutability. For example, the onset of Huntingtons Disease, a neurodegenerative disorder associated with somatic expansions of a trinucleotide coding STR, is delayed in individuals whose inherited alleles contain interruptions. Thus, interruptions that decrease mutation rate at some coding loci may broadly protect against deleterious phenotypes associated with locus instability. However, interruptions may themselves be deleterious at constrained loci, particularly at noncoding loci in gene regulatory elements, possibly disrupting the formation of secondary structures key to their function. We therefore hypothesized that the frequency of interruptions could depend on a locuss functional importance-at constrained loci, the fitness effects of expansions but also interruptions could be more deleterious than at neutral loci. To test this hypothesis, we examined the distribution of interruptions at [~]650,000 autosomal STRs. In the [~]2,500 3- or 6bp-motif coding STRs, we find that synonymous interruption density increases with purifying selection on the gene, while the opposite is true for missense-causing interruptions. In contrast, noncoding STRs in gene regulatory elements harbor fewer interruptions than those unassociated with function and putatively evolving neutrally. Our findings indicate that the abundance of interruptions may be partially explained at coding STRs by the benefit of lower instability. In contrast, maintaining a minimum core stretch of uninterrupted repeat may be key to the function of noncoding STRs that fall within regulatory elements, outweighing the benefits of stability.
- organism: human
- assay: DNA methylation
- assay: whole-genome sequencing
- research focus: chromatin & epigenetic regulation
- research focus: gene regulatory network inference
- research focus: cell type annotation
- research focus: clustering
- approach: statistical model
- Citations
- 1
- FWCI
- 2.46
- Field percentile
- top 14%
Reproducibility ledger
Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.
Sign in to file a reproducibility report.
Related papers
- Massive variation of short tandem repeats with functional consequences across strains of Arabidopsis thaliana.
Maximilian Oliver Press, Rajiv C. McCoy, … Christine Queitsch·Genome ResearchPeer-reviewed·Aug 1, 2018
- Genome-wide selection inference at short tandem repeats
Bonnie B. Huang, Arun Durvasula, … Melissa Gymrek·PLoS GeneticsPeer-reviewed·Dec 1, 2025
- The Mutational Dynamics of Short Tandem Repeats in Large, Multigenerational Families
Cody J. Steely, W. Scott Watkins, … Lynn B. Jorde·Genome biologyPeer-reviewed·Dec 12, 2022
- Short Tandem Repeats of Human Genome Are Intrinsically Unstable in Cultured Cells in vivo
Yuzhe Liu, Jinhuan Li, Qiang Wu·GenePeer-reviewed·Jun 4, 2023
- DNA polymerase stalling at structured DNA constrains the expansion of Short Tandem Repeats
P. Murat, G. Guilbaud, J. E. Sale·bioRxiv·Jun 20, 2020
- Interpreting short tandem repeat variations in humans using mutational constraint
Melissa Gymrek, Thomas Willems, … Yaniv Erlich·Nature GeneticsPeer-reviewed·Sep 11, 2017