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. 2018 Jan 22;28(2):249–261.e4. doi: 10.1016/j.cub.2017.12.020

Figure 3.

Figure 3

Double-Strand Break Processing

(A and B) Immunofluorescence staining of spermatocyte chromosome spreads of Smc1β+/+, Smc1β−/−, and Smc1β−/−,1a mice, probed with anti-SYCP3 (red) for AEs/LEs and anti-RAD51 (A) or anti-DMC1 (green; B) as indicated for DNA double-strand break repair foci.

(C) Graph showing numbers of RAD51 foci in pachytene stage cells (n = 25, 27 RAD51 foci ± 2.949 SD, Smc1β+/+; n = 56, 35 RAD51 foci ± 7.045 SD, Smc1β−/−; n = 26, 26 RAD51 foci ± 7.184 SD, Smc1β−/−,1a). The p values between all genotypes are <0.0001 except between Smc1β+/+ and Smc1β−/−,1a (p = 0.429).

(D) Graph showing numbers of DMC1 foci in pachytene stage cells. (n = 140, 23 DMC1 foci, ±1.89 SD, Smc1β+/+; n = 100, 42 DMC1 foci ± 5.89, Smc1β−/−; n = 150, 25 DMC1 foci ± 6.184, Smc1β−/−,1a). The p values between all genotypes are <0.0001 except between Smc1β+/+ and Smc1β−/−,1a (p = 0.258).

(E) Spermatocyte chromosome spreads of Smc1β+/+, Smc1β−/−, and Smc1β−/−,1a mice, probed with anti-SYCP3 (red) for AEs/LEs and anti-MLH1 for late recombinational nodule.

(F) Graphical representation of number of MLH1 foci in Smc1β+/+ and Smc1β−/−,1a spermatocytes. (Smc1β+/+: n = 18, 29 MLH1 foci ± 2.029 SD; Smc1β−/−,1a: n = 36, 22 MLH1 foci ± 3.713; p < 0.0001 according to unpaired t test; scale bar, 5 μm).

See also Figures S4 and S7.