Fig. 6. Restoration of spermatogenic defects in Scmh1^-/- testes by Phc2 mutation. (A) Restoration of morphological defects in Scmh1^-/- testes by Phc2 mutation. (B) Restoration of fertility in Scmh1^-/-;Phc2^-/- mice. Results from ten mice with respective genotypes were summarized. (C) Significant reduction of apoptotic outbursts in Scmh1^-/-;Phc2^-/- testes compared with Scmh1^-/- single mutants. (Left) Incidence of apoptosis was examined in wild-type, Scmh1^-/- and Scmh1^-/-;Phc2^-/- testes at day 19 pp by TUNEL staining. (Right) Three hundred seminiferous tubules derived from five mice with respective genotypes were analyzed for the presence of TUNEL-positive cells and the results were summarized. (D) Restoration of spermatocytes, in which dimethylated H3-K9 was enriched at the XY body in Scmh1^-/-;Phc2^-/- testes (left). Frequency of spermatocytes, in which dimethylated H3-K9 was accumulated on the XY body, was summarized (right). (E,F) Frequency of spermatocytes, in which monomethylated H3-K9 was enriched at (E) and phosphorylated pol II was excluded from (F) the XY body in Scmh1^-/-;Phc2^-/- testes was compared.