Embryonic diapause

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.[3] Many different factors can induce embryonic diapause, such as the time of year, temperature, lactation and supply of food.[3]

Embryonic diapause is a relatively widespread phenomenon outside of mammals, with known occurrence in the reproductive cycles of many insects, nematodes, fish, and other non-mammalian vertebrates.[6] It has been observed in approximately 130 mammalian species,[7] which is less than two percent of all species of mammals.[8] 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.[5]

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.[8][9]

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.[2] While much of the molecular regulation involved in activating dormant blastocysts has been characterized, little widely applicable characterization is available regarding entry into diapause, and the conditions which enable a blastocyst to remain dormant. Once the embryo exits diapause arrest and resumes regular development, no adverse effects are observed.[10]

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.[11] Hormones relating to the failed implantation also contribute to the embryonic arrest.[9]

There are two distinct forms of embryonic diapause, characterized by different conditions of onset. Facultative diapause occurs in response to certain environmental or metabolic stressors, such as drastic changes in temperature, feeding, or lactation.[10] Obligate diapause occurs regularly in the reproductive cycle of the affected species, and is often associated with seasonal changes and photo-period.[10]

Facultative diapause

Mechanism of facultative embryonic diapause

Facultative diapause is regulated by several factors, including the maternal environment and ovarian competency, the pituitary gland, and metabolic stress and lactation.[2]

With regards to the many other regulators of this form of diapause, in placental mammals, facultative diapause is most often the result of fertilization shortly following the birth of a previous litter, The consequential pups suckling during lactation promotes prolactin to be released. This in turn reduces progesterone secretion from the corpus luteum in a pregnant female. The corpus luteum is a temporary endocrine organ that is formed from the leftover cells from the ovarian follicle in the ovary, once it has released a mature ovum. The main function of the corpus luteum is to secrete progesterone during pregnancy in order to maintain the uterine environment needed. Prolactin acting on the corpus luteum causes the progesterone level to be below optimal concentration and therefore induces embryonic facultative diapause.

Each species that undergoes facultative diapause tends to have a specific developmental stage, that is genetically determined, in which this process is initiated. This form of diapause is most well studied in rodents and marsupials[2] but has been identified in many other species, including non-mammals. It is not clear how well the mechanisms studied for the onset, maintenance and release from facultative diapause in the rodent model apply to these other species.

Embryonic stem cells (ESCs) have the potential to allow for further understanding of the mechanisms controlling embryonic diapause.[13] This is because the ESCs and diapausing blastocysts having very similar transcriptome profiles.[13] ESCs are derived from the undifferentiated inner mass cells of blastocysts of an embryo – with the capability of continual proliferation in vitro.[13] ESCs are mostly derived from mouse models, at the point where the ESCs are at optimal efficiency and are able to enter diapause.[3]

Both diapausing blastocysts and ESCs have transcriptome profile similarities, including downregulation of metabolism, biosynthesis and gene expression pathways.[3] These similarities allow for the potential to use ESCs as a cellular model to identify the molecular factors which regulate embryonic diapause.[13]

• Weddell seal#Breeding