Сүтқоректілердің даму стратегиясы: Жұмырқакүштің тоқтауы

Evolutionary reproductive strategy of mammals

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 G0 or G1 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.

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 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.

All multicellular organisms, from their conception, begin as a small number of cells and only grow and develop as those cells divide. In organisms which are capable of embryonic diapause, in non ideal reproductive conditions, there is a cessation of cellular division which prevents the embryo from growing and maturing, delaying the maturation of the embryo until conditions are ideal enough to promote the survival of the offspring, and in some cases, the mother. Regulation of the cell cycle as it relates to embryonic diapause has been linked to the dacapo gene in the fruit fly, responsible for inhibiting the formation of cyclin E cdk2 complexes necessary for DNA synthesis. There is also evidence pointing to the upregulation of B cell translocation gene 1 (Btg1) in the mouse embryo during diapause, another known regulator of the cell cycle, responsible for inhibiting transition from G0/G1. Other studies have demonstrated, inversely, the lack of involvement of more common regulators of the cell cycle such as p53 within the placental model of embryonic diapause. Specifically within placental embryonic diapause, this cessation is led by the intentional failure of the blastocyst to implant in the uterine wall, which is an essential component in developmental progression in these species. Hormones relating to the failed implantation also contribute to the embryonic arrest. 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. After the vernal equinox, the photoperiod is greater than 12 hours. This decreases the production of melatonin in the pineal gland and, therefore, increases the prolactin and progesterone production in the pituitary gland and corpus luteum respectively. The increase in prolactin induces expression of the gene Odc (ornithine decarboxylase). The Odc gene produces the ODC protein, a rate limiting enzyme in the production of the polyamine, putrescine, within the uterine environment. The presence of putrescine may indicate a role in inducing the escape of the embryo from obligate diapause.

Embryonic stem cells (ESCs) have the potential to allow for further understanding of the mechanisms controlling embryonic diapause. This is because the ESCs and diapausing blastocysts having very similar transcriptome profiles. ESCs are derived from the undifferentiated inner mass cells of blastocysts of an embryo – with the capability of continual proliferation in vitro. ESCs are mostly derived from mouse models, at the point where the ESCs are at optimal efficiency and are able to enter diapause. Both diapausing blastocysts and ESCs have transcriptome profile similarities, including downregulation of metabolism, biosynthesis and gene expression pathways. These similarities allow for the potential to use ESCs as a cellular model to identify the molecular factors which regulate embryonic diapause.