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

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...

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Bibliographic Details
Published in:PLoS genetics 2009-02, Vol.5 (2), p.e1000393-e1000393
Main Authors: Bolcun-Filas, Ewelina, Hall, Emma, Speed, Robert, Taggart, Mary, Grey, Corinne, de Massy, Bernard, Benavente, Ricardo, Cooke, Howard J
Format: Article
Language:English
Subjects:
Animals
Cell Biology
Cellular proteins
Chromosome Pairing
Developmental Biology/Germ Cells
DNA Repair
Female
Gametogenesis
Gene mutations
Genes
Genetic aspects
Genetic diversity
Genetics
Genetics and Genomics/Chromosome Biology
Genomes
Health aspects
Human genetics
Infertility
Life Sciences
Male
Meiosis
Mice
Mice, Inbred C57BL
Mice, Knockout
Mutation
Nuclear Proteins - genetics
Nuclear Proteins - metabolism
Physiological aspects
Protein Binding
Proteins
Rad51 Recombinase - genetics
Rad51 Recombinase - metabolism
Recombination, Genetic
Spermatocytes - cytology
Spermatocytes - metabolism
Synaptonemal Complex - genetics
Synaptonemal Complex - metabolism
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Summary: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.
ISSN:1553-7404
1553-7390
1553-7404
DOI:10.1371/journal.pgen.1000393