Embryonic diapause (delayed implantation in mammals) is a reproductive strategy used by a number of animal species across different biological classes. In more than 130 types of mammals where this takes place, the process occurs at the blastocyst stage of embryonic development, and is characterized by a dramatic reduction or complete cessation of mitotic activity, arresting most often in the G<sub>0</sub> or G<sub>1</sub> phase of division.
In placental embryonic diapause, the blastocyst does not immediately implant in the uterus after sexual reproduction has resulted in the zygote, but rather remains in this non-dividing state of dormancy until conditions allow for attachment to the uterine wall to proceed as normal. As a result, the normal gestation period is extended for a species-specific time.
Diapause provides a survival advantage to offspring, because birth or emergence of young can be timed to coincide with the most hospitable conditions, regardless of when mating occurs or length of gestation; any such gain in survival rates of progeny confers an evolutionary advantage.
Evolutionary significance
Organisms which undergo embryonic diapause are able to synchronize the birth of offspring to the most favorable conditions for reproductive success, irrespective of when mating took place. It has been observed in approximately 130 mammalian species, which is less than two percent of all species of mammals. These include certain pinnipeds, rodents, bears, armadillos, mustelids (e.g. weasels and badgers), and marsupials (e.g. kangaroos). Some groups only have one species that undergoes embryonic diapause, such as the roe deer in the order Artiodactyla.
Experimental induction of embryonic discontinuous development within species which do not spontaneously undergo embryonic diapause in nature has been achieved; reversible developmental arrest was successfully demonstrated. This may be evidence for the evolutionary significance of this phenomenon, with latent capacity for diapause potentially present in a much wider segment of species than known to occur naturally.
General mechanism
Organisms which can stop their cellular division (embryonic diapause) can prevent an embryo from growing. Non-ideal reproductive conditions are what initiate this process, as delaying embryo maturation promotes survival of offspring and the parent.
Placental embryonic diapause in particular is an essential component of developmental progression in these species. This cessation is led by the intentional failure of the blastocyst to implant the uterine wall. Hormones relating to the failed implantation also contribute to the embryonic arrest.
Regulation of the cell cycle as it relates to embryonic diapause has been linked to the dacapo gene in the fruit fly. This gene inhibits the formation of Cyclin E/Cdk2 complexes, which is necessary for DNA synthesis. Another known regulator of the cell cycle, the B cell translocation gene 1 BTG1, has shown upregulation in mouse embryos during diapause, responsible for inhibiting transition from G<sub>0</sub>/G<sub>1</sub> (G0 phase, G1 phase). Inversely, other studies have demonstrated that common regulators of the cell cycle lack involvement, such as P53, within the placental model of embryonic diapause.
Prior to the vernal equinox, the photoperiod is less than 12 hours. This increases the production of melatonin in the pineal gland. Due to the inhibitory relationship between melatonin and prolactin, this increase in melatonin decreases prolactin secretion from the pituitary gland. The decrease in prolactin consequently decreases progesterone production in the corpus luteum, preventing development of the blastocyst. This induces embryonic diapause.