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Transposons make up a significant part of genomes of various organisms. Therefore, it is believed that transposition played a major evolutionary role in speciation by changing genome sizes and modifying gene expression patterns. For example, in bacteria, transposition can lead to conferring antibiotic resistance. Movement of transposable elements within the genetic pool of pathogenic bacteria can aid in transfer of antibiotic-resistant genetic elements. In eukaryotes, transposons can carry out...
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A population genetics theory for piRNA-regulated transposable elements.

Siddharth S Tomar1, Aurélie Hua-Van1, Arnaud Le Rouzic1

  • 1Université Paris-Saclay, CNRS, IRD, UMR EGCE, 12 Route 128, Gif-sur-Yvette, 91190, France.

Theoretical Population Biology
|March 2, 2023
PubMed
Summary
This summary is machine-generated.

Transposable elements (TEs) are regulated by a "trap model" involving piRNAs. New population genetics models show TE dynamics are more stochastic and less predictable than previously thought.

Keywords:
ModelSimulationsTransposition regulationTrap modelpiRNA clusters

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Area of Science:

  • Genetics
  • Evolutionary Biology
  • Population Genetics

Background:

  • Transposable elements (TEs) are mobile DNA sequences that can proliferate within genomes.
  • TE copy numbers are typically limited by transposition regulation or natural selection against deleterious copies.
  • Recent findings suggest piRNA-mediated regulation, activated by TE insertions into piRNA clusters (the 'trap model'), is a key mechanism.

Purpose of the Study:

  • To develop and analyze population genetics models incorporating the TE regulation 'trap model'.
  • To investigate how this 'trap model' influences TE copy number equilibria and invasion dynamics.
  • To compare the 'trap model' predictions with traditional transposition-selection equilibrium models.

Main Methods:

  • Derived new population genetics models based on the piRNA cluster 'trap model'.
  • Proposed three sub-models considering different selective pressures (neutral or deleterious) on genomic and cluster TE copies.
  • Derived analytical expressions for maximum/equilibrium copy numbers and cluster frequencies.
  • Compared model predictions with numerical simulations.

Main Results:

  • TE dynamics under the 'trap model' differ significantly from traditional models.
  • In the neutral model, equilibrium is reached via complete transposition silencing, independent of transposition rate.
  • Deleterious genomic TEs (but not cluster TEs) lead to elimination without long-term equilibrium.
  • Deleterious TEs result in a non-monotonic invasion with a copy number peak before decline.
  • Model predictions align well with simulations, except when drift or linkage disequilibrium is high.

Conclusions:

  • The 'trap model' introduces substantial stochasticity and reduces repeatability in TE dynamics compared to traditional models.
  • TE regulation via piRNA clusters presents a unique evolutionary dynamic.
  • Understanding these dynamics is crucial for comprehending genome evolution and TE-host interactions.