Nature Genetics
27, 271 - 276 (2001)
doi:10.1038/85830
Recombinational DNA double-strand breaks in mice precede synapsisShantha K. Mahadevaiah1, James M.A. Turner1, Frédéric Baudat2, Emmy P. Rogakou3, Peter de Boer4, Josefa Blanco-Rodríguez5, Maria Jasin2, Scott Keeney2, William M. Bonner3
& Paul S. Burgoyne11
Division of Developmental Genetics, National Institute for Medical Research, London, UK. 2
Memorial Sloan-Kettering Cancer Center, New York, New York, USA. 3
Laboratory of Molecular Pharmacology, NCI, National Institutes of Health, Bethesda, Maryland, USA. 4
Laboratory of Genetics, Wageningen Institute of Animal Sciences, Wageningen, The Netherlands. 5
Department of Cell Biology, School of Medicine, Valladolid University, Valladolid, Spain.
Correspondence should be addressed to Paul S. Burgoyne pburgoy@nimr.mrc.ac.ukIn Saccharomyces cerevisiae, meiotic recombination is initiated by Spo11-dependent double-strand breaks (DSBs), a process that precedes homologous synapsis. Here we use an antibody specific for a phosphorylated histone ( -H2AX, which marks the sites of DSBs) to investigate the timing, distribution and Spo11-dependence of meiotic DSBs in the mouse. We show that, as in yeast, recombination in the mouse is initiated by Spo11-dependent DSBs that form during leptotene. Loss of -H2AX staining (which in irradiated somatic cells is temporally linked with DSB repair) is temporally and spatially correlated with synapsis, even when this synapsis is 'non-homologous'.
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