Proliferation and migration of primordial germ cells during compensatory growth in mouse embryos

TLDR

Mitomycin C was injected intraperitoneally into pregnant mice at embryonic days 6.75–7.0 to arrest cell proliferation during the primitive streak stage. The treatment caused severe depletion of primordial germ cells early in development, resulting in poor neonatal growth, high mortality, and long‑term fertility deficits due to impaired germ cell migration, gonadal development, and gametogenesis.

Abstract

Primitive-streak-stage mouse embryos were treated with Mitomycin C injected intraperitoneally into pregnant females at 6.75--7.0 days post coitum. The newborn mice developed poorly and mortality was high during the suckling period. Many weaned survivors showed impaired fertility and poor breeding performance. Histological examination revealed a paucity of germ cells in the adult gonads. The deficiency was mainly caused by a severe reduction of the primordial germ cell population in early embryonic life, which was not fully compensated for during the compensatory growth phase of the Mitomycin C-treated embryo. Also contributing to such impaired fertility were retarded migration of the primordial germ cells into the genital ridges, poor development of the foetal gonad and secondary loss of the germ cells during gametogenesis in males.