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Emx2  deletion impairs the growth and maintenance of the genital ridge. However, its role in subsequent germ cell differentiation during embryonic stages is unknown. Using a tamoxifen-inducible Cre-loxP mouse model ( Emx2  flox/flox ,  Cre-ER  TM , hereafter called as  Emx2  knockdown), we showed that germ cell differentiation was impaired in  Emx2- knockdown testes. Representative characteristics of male germ cell differentiation, including a reduced ability to form embryonic germ (EG) cell colonies  in vitro , down-regulation of pluripotency markers and G1/G0 arrest, did not occur in  Emx2- knockdown testes. Furthermore, FGF9 and NODAL signalling occurred at abnormally high levels in  Emx2- knockdown testes. Both blocking FGF9 signalling with SU5402 and inhibiting NODAL signalling with SB431542 allowed germ cells from  Emx2- knockdown testes to differentiate  in vitro . Therefore, EMX2 in somatic cells is required to trigger germ cell differentiation in XY foetuses, posterior to its previously reported role in the growth and maintenance of the genital ridge.

Critical role of Emx2 in the pluripotency – differentiation transition in male gonocytes via regulation of FGF9/NODAL pathway