Cited by 44Fungal and yeast genetics researchChromosomal and Genetic VariationsDNA Repair Mechanisms

Breaking a species barrier by enabling hybrid recombination

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Bozdag, G. Ozan, Ono, Jasmine, Denton, Jai A., Karakoc, Emre, Hunter, Neil, Leu, Jun-Yi, Greig, Duncan·2021·Current Biology

Abstract

Hybrid sterility maintains reproductive isolation between species by preventing them from exchanging genetic material 1. Anti-recombination can contribute to hybrid sterility when different species' chromosome sequences are too diverged to cross over efficiently during hybrid meiosis, resulting in chromosome mis-segregation and aneuploidy. The genome sequences of the yeasts Saccharomyces cerevisiae and Saccharomyces paradoxus have diverged by about 12% and their hybrids are sexually sterile: nearly all of their gametes are aneuploid and inviable. Previous methods to increase hybrid yeast fertility have targeted the anti-recombination machinery by enhancing meiotic crossing over. However, these methods also have counteracting detrimental effects on gamete viability due to increased mutagenesis 2 and ectopic recombination 3. Therefore, the role of anti-recombination has not been fully revealed, and it is often dismissed as a minor player in speciation 1. By repressing two genes, SGS1 and MSH2, specifically during meiosis whilst maintaining their mitotic expression, we were able to increase hybrid fertility 70-fold, to the level of non-hybrid crosses, confirming that anti-recombination is the principal cause of hybrid sterility. Breaking this species barrier allows us to generate, for the first time, viable euploid gametes containing recombinant hybrid genomes from these two highly diverged parent species.

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Crossref · 10.1016/j.cub.2020.12.038

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  • Confirmation that a gene participates in an incompatibility will ultimately require experimental validation.

    “Confirmation that a gene participates in an incompatibility will ultimately require experimental validation (see, e.g., Bozdag et al. 2021)”

    From Finding Hybrid Incompatibilities Using Genome Sequences from Hybrid Populations (2021) · cites this paper as Bozdag et al. 2021

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Authors
Bozdag, G. O., Ono, J., Denton, J. A., Karakoc, E., Hunter, N., Leu, J.-Y., & Greig, D.
Affiliations
  • Georgia Institute of Technology (US)
  • University College London (GB)
  • Okinawa Institute of Science and Technology Graduate University (JP)
  • Howard Hughes Medical Institute (US)
  • Institute of Molecular Biology, Academia Sinica (TW)
  • Max Planck Institute for Evolutionary Biology (DE)
Corresponding author
Ono, Jasmine
Venue
Current Biology
Publisher
Elsevier BV
Published
2021-02
Volume
31
Issue
4
Pages
R180-R181
ISSN
0960-9822 (ISSN-L)
OpenAlex
W3131052818
Cited by
43
References
9
Citations by year
2026: 4 · 2025: 10 · 2024: 4 · 2023: 6 · 2022: 9 · 2021: 9 · 2018: 1
FWCI
2.20
Type
journal article
Language
en
Open access
Locations
  • Current Biology (publishedVersion)
  • PubMed (publishedVersion)
  • UCL Discovery (University College London) (submittedVersion)
  • Zenodo (CERN European Organization for Nuclear Research) (submittedVersion, cc-by)
  • Zenodo (CERN European Organization for Nuclear Research) (cc-by)
Funders
  • Leverhulme Trust (RPG-2017-438)
  • Royal Society (ALTF 265-2017)
  • Max-Planck-Institut für Evolutionäre Anthropologie
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
  • Life Sciences › Agricultural and Biological Sciences › Plant Science › Chromosomal and Genetic Variations
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Keywords
hybrid sterility, hybrid fertility, Saccharomyces cerevisiae, Saccharomyces paradoxus, meiotic crossover, Sgs1, MSH2, meiotic recombination, reproductive isolation, speciation, aneuploidy, chromosome missegregation
MeSH terms
Aneuploidy, Hybridization, Genetic, Meiosis, Recombination, Genetic, Saccharomyces, Saccharomyces cerevisiae, Chromosome Segregation, Saccharomyces cerevisiae Proteins, MutS Homolog 2 Protein, RecQ Helicases

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