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Mathematical and live meningococcal models for simple sequence repeat dynamics - coherent predictions and
Kristian Alfsnes1, Xavier Raynaud2, Tone Tønjum1
1Department of Microbiology, University of Oslo, Oslo, Norway; Department of Microbiology, Oslo University Hospital (Rikshospitalet), Oslo, Norway.
Plos One
|July 8, 2014
Summary
Simple sequence repeat (SSR) instability influences evolvability, with mathematical models and meningococcal strain studies revealing factors shaping SSR tract length. Genetic instability and selection pressures impact SSR evolution, particularly in antibiotic resistance genes.
Area of Science:
- Microbiology
- Genetics
- Evolutionary Biology
Background:
- Simple sequence repeats (SSRs) are prone to instability, influencing genetic variation and evolvability.
- Opposing selective pressures and factors affecting genetic instability constantly shape SSR tract length.
- SSR instability can modulate gene expression, as seen in antibiotic resistance switching.
Purpose of the Study:
- To mathematically model and experimentally investigate the factors influencing SSR tract length evolution.
- To understand how SSR instability affects the ON/OFF switching of antibiotic resistance in meningococcal strains.
- To explore the roles of selection, genetic instability, and mutational biases in SSR evolution.
Main Methods:
- Developed a mathematical model incorporating direct selection, tract length-dependent (α), and tract length-independent factors (β).
- Monitored SSR instability in a panel of live Neisseria meningitidis strains, focusing on spectinomycin resistance switching.
- Assessed the instability of homopolymeric SSRs (5-13 guanine nucleotides) in wildtype and mismatch repair-deficient backgrounds.
Main Results:
- The mathematical model indicated that selection (α) favors shorter tracts, while other factors (β) drive towards a normal distribution.
- Insertion and deletion biases were observed to skew SSR allelic distributions.
- SSR tract length and mismatch repair deficiency significantly influenced genetic instability; an insertion bias was noted in tracts ≤G10.
- An inverse correlation between tract-encoded amino acids and growth under selection demonstrated a limitation to SSR expansion in essential genes.
Conclusions:
- SSR evolution is shaped by a complex interplay of selection, genetic instability, and mutational biases.
- Mismatch repair deficiency and SSR length are critical determinants of SSR genetic instability.
- Functional constraints in essential genes limit SSR expansion, providing insights into evolutionary mechanisms.
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