Embryonic Diapause Delays Pregnancy in Some Mammals

Some mammals can actually delay the onset of their pregnancies, and researchers have now been able to identify the molecular mechanism behind this remarkable ability.

The phenomenon, known as embryonic diapause, is a temporary state of suspended animation that occurs when environmental conditions are not favorable to the survival of the mother and the newborn. The new study reveals that the genes are responsible for pausing and resuming a pregnancy.

After an egg is fertilized, it forms a cluster of cells called a blastocyst, which implant in the walls of the mother's uterus. During diapause, however, the blastocyst is prevented from implanting and preserved in an inactive state until pregnancy resumes. Yet exactly how this process occurs is a mystery.

Sudhansu Dey, of Cincinnati Children's Research Foundation, and colleagues were studying the process of embryo implantation in mice when they noticed that a gene called MSX1 was very active just before implantation. They began to suspect that it might play a role in diapause, Dey said, according to LiveScience.

To investigate further, Dey's team used hormones to induce pregnancy delays in mice, mink and Tammar wallabies. During this delayed state, the researchers measured how active the MSX1 gene and other related genes were in generating protein-making instructions. Then, they imaged tissue from the animals to see where the gene was active. Finally, they tested whether these genes were being made into proteins.

Researchers found that the MSX genes were more active when pregnancies were delayed. They also found this was true for all three animals. The genes were primarily active in epithelial cells, the type of cells that line body cavities such as the interior of the uterus. The experiments also confirmed that these genes were indeed making proteins.

Researchers hope they can extend this finding to other mammals, including polar bears.

Ultimately, a deeper understanding of diapause could have implications for humans, Dey said. "If we keep MSX1 maintained at higher levels in human [women], maybe we can extend the receptive phase" such as fertilization. However, he added that any extensions regarding the experiment would take many years to achieve.

The findings are published online this month in the journal Open Biology.