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PLoS Genet. 2009 Feb;5(2):e1000393. doi: 10.1371/journal.pgen.1000393. Epub 2009 Feb 27.

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

Author information

1
MRC Human Genetics Unit and Institute of Genetics and Molecular Medicine, Western General Hospital, Edinburgh, United Kingdom.

Erratum in

  • PLoS Genet. 2009 Apr;5(4). doi: 10.1371/annotation/50260271-aed9-4316-b09a-304591b0cba5. Hall, Emma [added].

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.

PMID:
19247432
PMCID:
PMC2640461
DOI:
10.1371/journal.pgen.1000393
[Indexed for MEDLINE]
Free PMC Article

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