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Evolution of an MCM complex in flies that promotes meiotic crossovers by blocking BLM helicase

Kathryn P Kohl1, Corbin D Jones, Jeff Sekelsky

  • 1Curriculum in Genetics and Molecular Biology, University of North Carolina, Chapel Hill, NC 27599, USA.

Science (New York, N.Y.)
|December 11, 2012
PubMed

Insights

In flies, minichromosome maintenance (MCM) proteins replaced the Msh4-Msh5 complex to ensure meiotic crossover generation. This MCM complex evolved to facilitate crossovers, overcoming the loss of Msh4-Msh5.

Area of Science:

  • Genetics
  • Molecular Biology
  • Evolutionary Biology

Background:

  • Meiotic crossover formation in eukaryotes often involves the Msh4-Msh5 heterodimer inhibiting anti-crossover helicases.
  • The Msh4 and Msh5 proteins are absent in flies like Drosophila and Glossina.

Purpose of the Study:

  • To identify the proteins that functionally replace the Msh4-Msh5 heterodimer in Drosophila for meiotic crossover generation.
  • To investigate the evolutionary origin and function of these replacement proteins.

Main Methods:

  • Genetic analysis of Drosophila mutants for key genes (rec, mei-217, mei-218).
  • Biochemical interaction studies to identify protein complexes.
  • Comparative genomics to trace the evolutionary history of MCM proteins.

Main Results:

  • A complex of minichromosome maintenance (MCM) proteins, including REC (MCM8 ortholog) and novel proteins MEI-217/MEI-218, was identified.
  • REC evolved under positive selection in flies and interacts with MEI-217/MEI-218, a metazoan-specific MCM protein.
  • Mutations in rec, mei-217, or mei-218 reduced meiotic crossovers, but this was rescued by removing the Bloom syndrome helicase (BLM) ortholog.

Conclusions:

  • Minichromosome maintenance (MCM) proteins were repurposed to form a novel complex that substitutes for the meiotic pro-crossover function of Msh4-Msh5 in flies.
  • This MCM complex plays a crucial role in regulating meiotic crossovers in the absence of Msh4-Msh5.

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