Embryonic diapause was first identified over 150 years ago, but many questions still remain about how the external and hormonal controls of embryonic diapause translate into how the uterus conveys information to the embryo. Current evidence suggests that the control of diapause is mediated by components of the uterine secretions. However, the identity of the essential signalling molecule(s) is unknown. The mouse (Mus musculus), the mink (Neovison vison) and the tammar wallaby (Macropus eugenii) are the three most extensively studied mammalian diapause species. Despite differences in the external and hormonal control of diapause between these three species, we have now found that there is conservation of numerous molecular factors around diapause and reactivation. This was first suggested via the conserved expression of various growth factors. The first evidence for a conserved mechanism resulted from a study on the muscle segment homeobox transcription factor (MSX) in the uterus during diapause, whose expression is conserved amongst the mouse, mink and wallaby. Following this was the evidence that inhibition of polyamines induces entry into diapause in both the mink and mouse. Thus, although the signalling mechanisms via which the uterus is induced into diapause vary amongst species, the molecular communication that occurs between the uterus and the embryo to control diapause is conserved. Given that these mechanisms are conserved across varying taxa, this implies a universal mechanism for maintaining embryo health amongst all mammals. New technologies are now allowing us to examine diapause from a global perspective and to increase our knowledge of this enigmatic stage of pregnancy.
© Third International Symposium on Embryonic Diapause