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Because the DNA segments are cut and reorganized in a direction-specific manner, site-specific recombination has emerged as an efficient genetic engineering technique. Flippase and Cyclization recombinases or Flp and Cre, respectively, are two members of the tyrosine recombinase family derived from bacteriophages, that are used to mediate site-specific DNA insertions, deletions, and targeted expression of proteins in mammalian cell lines.
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The Recombination Hotspot Paradox: Co-evolution between PRDM9 and its target sites.

Francisco Úbeda1, Frédéric Fyon1, Reinhard Bürger2

  • 1Department of Biology, Royal Holloway University of London, Egham TW20 0EX, UK.

Theoretical Population Biology
|July 14, 2023
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Recombination hotspots, though self-destructive, persist in vertebrates due to a balance of mutation, gene conversion, and fertility selection. The gene PRDM9 influences hotspot activity, resolving the Recombination Hotspot Paradox.

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ChaosGene conversionIntragenomic conflictLimit cyclesMutationRed queen

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Area of Science:

  • Genetics and Evolutionary Biology
  • Population Genetics
  • Molecular Biology

Background:

  • Recombination hotspots are genomic regions with elevated recombination rates, primarily determined by the PRDM9 gene in vertebrates.
  • These hotspots are inherently self-destructive due to gene conversion, leading to a paradox where they are abundant despite their tendency to disappear.
  • The persistence of recombination hotspots challenges evolutionary theory, necessitating an explanation for their continuous presence.

Purpose of the Study:

  • To investigate the mechanisms that maintain the abundance of recombination hotspots in vertebrate genomes.
  • To resolve the Recombination Hotspot Paradox by modeling the interplay of evolutionary forces.
  • To understand the role of PRDM9 gene regulation in hotspot dynamics.

Main Methods:

  • Formulation of a co-evolutionary model incorporating sequence-specific gene conversion, fertility selection, and recurrent mutation.
  • Analysis of allelic frequency dynamics and their resulting oscillations.
  • Simulation of multiple alleles and multiple targets to assess their impact on genomic recombination probability.

Main Results:

  • The model demonstrates that oscillations in allelic frequencies lead to stable limit cycles, preventing hotspot extinction.
  • Fertility selection, when weaker than gene conversion, can resuscitate dying hotspots, maintaining their overall number.
  • Recurrent mutation balances hotspot death and resuscitation, ensuring their evolutionary persistence.
  • Multiple alleles and targets contribute to chaotic or asynchronous oscillations, stabilizing average genomic recombination probability.
  • PRDM9 expression levels correlate with the fraction of targets that become hotspots.

Conclusions:

  • The co-evolutionary model successfully explains the persistence of recombination hotspots, resolving the Recombination Hotspot Paradox.
  • The balance between mutation, gene conversion, and fertility selection is crucial for maintaining hotspot activity over evolutionary timescales.
  • PRDM9's regulatory role is key in modulating hotspot distribution and genomic recombination.
  • The study provides testable predictions regarding mutation probability, fertility selection, and hotspot longevity.