Figures for the Meiotic Recombination in the Mouse project.

Surface-spread spermatocyte nuclei were stained with a serum recognizing mouse Dmc1 and Rad51 (green) and with antibodies that recognizes a component of the mouse chromosome axis, Scp3 (red). Single-channel (A) and two-channel overlay (B) images of a wild Lack of Recombination Complexes in Spo11 mutants Spread spermatocyte nuclei were stained with anti-DMC1 antibodies (green) and with antibodies that recognize a component of the mouse chromosome axis, SYCP3 (red). A wild-type zygotene nucleus (A,B) shows numerous DMC1 foci along chromosome axes, whereas a Spo11 mutant nucleus (C, D) lacks detectable DMC1 foci.
Figure 3 DNA Damage-dependent and Independent Oocyte Loss Figure 3 DNA Damage-dependent and Independent Oocyte Loss Stages of oocyte development in wild type are diagrammed at the top, starting at early meiotic prophase in the fetal ovary. Meiotic arrest plus communication with somatic cells give rise to primordial follicles. Subsequent growth of follicles and oocytes is followed by resumption of meiosis, completion of the first division, and ovulation (not shown). Increased oocyte loss (gray arrows) in the Spo11 mutant is apparent during prenatal development and just after birth, during primordial follicle formation. More severe DNA damage-dependent oocyte loss occurs at/or prior to follicle formation in Dmc1-, Atm-, and Msh5-deficient animals.
Lagging chromosomes in ATM-deficient spermatocytes at metaphase I Lagging chromosomes in ATM-deficient spermatocytes at metaphase I Testis sections were immunostained with anti-tubulin antibodies to detect the spindle (green), and with DAPI (pseudocolored red). Arrowheads show examples of lagging chromosomes.