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Fig. 13. Schematic representation of PGC proliferation as function of developmental stage/
days after hatching in selected model fi shes: Upper panels: Left, Oryzias latipes , Right, Puntius
conchonius Lower left panel: Oreochromis niloticus and Lower right panel: Silurus meridionalis
(compiled from Saito et al. (2007), Kobayashi et al. (2004, 2008) Cek et al. (1998) and Liu et
al. (2008))
arrest, it progresses slowly to accumulate only about 65 and odd cells at
stage 39 (Kobayashi et al., 2004). Saito et al. (2007) have more elaborately
described the proliferation of PGCs in XX embryos, and the proliferation
is continued with intermittent divisions producing isolated daughter cells.
Two to four rounds of continuous divisions form cysts each with four, eight
and 16 cells, which subsequently enter meiosis synchronously. Interestingly,
the zenzai mutant medaka, a defect of slow intermittent division, eventually
leads to the depletion of PGCs in adult gonads of both sexes, despite the cyst
formation process remaining unaffected. Conversely, excessive proliferation
of PGCs occurs in the mutant hotei with Y3qoe mutation in amh receptor type
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