In Saccharomyces cerevisiae, meiotic recombination is initiated by Spo11-de
pendent double-strand breaks (DSBs), a process that precedes homologous syn
apsis. Here we use an antibody specific for a phosphorylated histone (gamma
-H2AX, which marks the sites of DSBs) to investigate the timing, distribut
ion 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 gamma -H2AX staining (which in irradiated s
omatic cells is temporally linked with DSB repair) is temporally and spatia
lly correlated with synapsis, even when this synapsis is 'non-homologous'.