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Effects of XRCC2 and RAD51B mutations on somatic and meiotic recombination in A rabidopsis thaliana
Author(s) -
Ines Olivier,
Degroote Fabienne,
Amiard Simon,
Goubely Chantal,
Gallego Maria E.,
White Charles I.
Publication year - 2013
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/tpj.12182
Subject(s) - rad51 , homologous recombination , biology , genetics , meiosis , saccharomyces cerevisiae , homologous chromosome , dna repair , flp frt recombination , mitotic crossover , genetic recombination , dna , recombination , gene
Summary Homologous recombination is key to the maintenance of genome integrity and the creation of genetic diversity. At the mechanistic level, recombination involves the invasion of a homologous DNA template by broken DNA ends, repair of the break and exchange of genetic information between the two DNA molecules. Invasion of the template in eukaryotic cells is catalysed by the RAD 51 and DMC 1 recombinases, assisted by a number of accessory proteins, including the RAD 51 paralogues. Eukaryotic genomes encode a variable number of RAD 51 paralogues, ranging from two in yeast to five in animals and plants. The RAD 51 paralogues form at least two distinct protein complexes, believed to play roles in the assembly and stabilization of the RAD 51‐ DNA nucleofilament. Somatic recombination assays and immunocytology confirm that the three ‘non‐meiotic’ paralogues of A rabidopsis, RAD 51B, RAD 51D and XRCC 2, are involved in somatic homologous recombination, and that they are not required for the formation of radioinduced RAD 51 foci. Given the presence of all five proteins in meiotic cells, the apparent absence of a meiotic role for RAD 51 B , RAD 51 D and XRCC 2 is surprising, and perhaps simply the result of a more subtle meiotic phenotype in the mutants. Analysis of meiotic recombination confirms this, showing that the absence of XRCC 2, and to a lesser extent RAD 51 B , but not RAD 51 D , increases rates of meiotic crossing over. The roles of RAD 51 B and XRCC 2 in recombination are thus not limited to mitotic cells.