The most prominent hypothesis for the evolutionary origin of imprinting is the parental conflict hypothesis, whereby paternally expressed imprinted genes are expected to promote fetal growth, while maternally expressed imprinted genes limit fetal growth. In support of this hypothesis, it is known that many imprinted genes act by regulating placental development and function. In this Issue, Amanda Sferruzzi-Perri and colleagues focus on how imprinted genes impact hormone production by the placenta by studying their role in the junctional zone (Jz), which is responsible for endocrine functions of the mouse placenta. The authors selectively delete the imprinting control region 1 (ICR1), which controls the paternally expressed genes Igf2, Ins2 and Igf2as, and the maternally expressed long non-coding RNA H19. The authors observe an expansion of the Jz that is associated with an increase in the number of endocrine cells due to increased proliferation. In addition, they report an increase in expression of the Jz hormone pregnancy-specific glycoprotein 23, but observe no effect on fetal weight. Finally, they find that ICR1 deletion also affects protein expression of IGF2 signalling factors in a sexually dimorphic manner. Together, these results demonstrate an important role for imprinted genes in the endocrine function of the placenta.
