Mutation of the mouse Syce1 gene disrupts synapsis and suggests a link between synaptonemal complex structural components and DNA repair

Ewelina Bolcun-Filas, Emma Hall, Robert Speed, Mary Taggart, Corinne Grey, Bernard de Massy, Ricardo Benavente, Howard J Cooke

Research output: Contribution to journalArticlepeer-review

Abstract

In mammals, the synaptonemal complex is a structure required to complete crossover recombination. Although suggested by cytological work, in vivo links between the structural proteins of the synaptonemal complex and the proteins of the recombination process have not previously been made. The central element of the synaptonemal complex is traversed by DNA at sites of recombination and presents a logical place to look for interactions between these components. There are four known central element proteins, three of which have previously been mutated. Here, we complete the set by creating a null mutation in the Syce1 gene in mouse. The resulting disruption of synapsis in these animals has allowed us to demonstrate a biochemical interaction between the structural protein SYCE2 and the repair protein RAD51. In normal meiosis, this interaction may be responsible for promoting homologous synapsis from sites of recombination.
Original languageEnglish
Pages (from-to)e1000393
JournalPLoS Genetics
Volume5
Issue number2
DOIs
Publication statusPublished - Feb 2009

Keywords

  • Animals
  • Chromosome Pairing
  • DNA Repair
  • Female
  • Gametogenesis
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Nuclear Proteins
  • Protein Binding
  • Rad51 Recombinase
  • Recombination, Genetic
  • Spermatocytes
  • Synaptonemal Complex

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