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Molecular Evolution of the Tre Recombinase
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PRDM9 and the evolution of recombination hotspots.

Francisco Úbeda1, Timothy W Russell1, Vincent A A Jansen1

  • 1School of Biological Sciences, Royal Holloway University of London, Egham, Surrey, TW20 0EX, UK.

Theoretical Population Biology
|January 21, 2019
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Summary

Recombination hotspots in mammals paradoxically persist despite self-inactivation. A new model shows weak selection can resurrect dying hotspots, explaining their abundance and genomic volatility.

Keywords:
Gene conversionHeteroclinic cyclesPRDM9Population geneticsRecombination hotspot paradoxViability selection

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Area of Science:

  • Genetics
  • Evolutionary Biology
  • Population Genetics

Background:

  • Recombination hotspots are non-uniformly distributed genomic regions crucial for mammalian genetic diversity.
  • Recombination initiates with double-strand breaks, paradoxically leading to hotspot inactivation and potential extinction.
  • The Recombination Hotspot Paradox describes the abundance of hotspots despite their self-inactivating nature.

Purpose of the Study:

  • To propose an alternative explanation for the Recombination Hotspot Paradox using a population genetics model.
  • To investigate the role of PRDM9-like genes and selection in hotspot dynamics.
  • To understand the evolutionary persistence and landscape volatility of recombination hotspots.

Main Methods:

  • Formulation of a population genetics model incorporating the mammalian recombination initiation mechanism (PRDM9-like genes).
  • Analysis of how weak selection influences the inactivation and re-activation (resurrection) of individual recombination hotspots.
  • Examination of genomic signatures, specifically selective sweeps, under varying levels of viability selection.

Main Results:

  • Weak selection allows individual recombination hotspots to become inactive (die) but prevents their extinction through re-activation (resurrection).
  • Rare variants and weak selection cause recombination sites to oscillate between active (hot) and inactive (cold) states.
  • Counter-intuitively, lower viability selection results in a harder selective sweep signature at recombination hotspots.

Conclusions:

  • The model provides a mechanism for hotspot persistence, reconciling empirical observations with theoretical expectations.
  • Weak selection and PRDM9-like gene dynamics explain hotspot resurrection, coexistence of hotspot types, and landscape volatility.
  • The findings offer insights into PRDM9 evolution and the low conservation of recombination hotspots between species.