embryonic development can actually take an "intermission"! "cell": press the on-off button and the embryo will sleep
2024-09-29
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▎edited by wuxi apptec content team
from a fertilized egg to a complete individual, a complex embryonic development process is required. perhaps we would think that once the embryo begins to develop, it will rush forward without any slack, pushing forward each step step by step. but in fact, embryonic development involves a series of cell differentiation and special events, including a dormant period that pauses development.
according to the waddington model, the development of the embryo is like a small ball rolling down a hillside, from an undifferentiated unstable state on the top of the mountain to the basin where it becomes a terminally differentiated form. however,this ball rolling process can be paused. many mammals have evolved mechanisms to temporarily delay embryonic development, arresting the embryo at the blastocyst stage and preserving the embryo.。
this phenomenon of embryonic dormancy can be triggered by hormonal changes, starvation and other factors. under adverse conditions, the suspension of embryonic development can help improve the survival rate of the embryo and mother. during this period, the embryo will be in a free-floating state. when the conditions are favorable, the embryo will restart the development process. although scientists have observed this phenomenon in many mammals, most studies believe that human embryos do not have a developmental "dormant period."in a new study in the journal cell, scientists from the max planck institute of molecular genetics made a bold attempt to artificially introduce some external intervention to see if they could trigger a pause in human embryonic development. turn out,molecular mechanisms controlling embryonic 'dormant periods' may also potentially play a role in human embryos, which means that future researchers can regulate embryonic development in vitro and increase the success rate of ivf embryos.according to the paper, due to ethical issues, the new study did not directly select human embryos as experimental subjects, but used a blastocyst model based on human stem cells to conduct exploration. in previous studies, the authors found that the mtor pathway is a major player in mouse embryonic development.simply inhibiting mtor signaling in mouse blastocysts alone is enough to cause a development-like pause in the embryo, and can even limit the development of the blastocyst for weeks.。based on these findings, the authors tried to add an mtor inhibitor to the human stem cell blastocyst model. compared with the untreated control group, mtor-downregulated blastocysts had smaller blastocysts and a higher number of trophectoderm-like cells. few. these differences indicate that the development process of the blastocyst is delayed and inhibited.▲research diagram(image source: reference [2])in addition, after mtor is down-regulated, the expression of proteins related to blastocyst implantation is reduced, reducing the chance of the blastocyst implanting in the endometrial cell layer and further limiting the embryonic development process. "this means that we can induce dormancy-like phenomena in human embryos by changing mtor." dr. aydan bulut-karslioglu, the corresponding author of the study, said,this dormancy is reversible. as long as the mtor signaling pathway is reactivated, the blastocyst model will enter normal developmental steps.。the authors believe that humans, like other mammals, still have internal mechanisms to slow down embryonic development, but they do not actively activate this mechanism during pregnancy. but as long as this ability exists, it is expected to have an important impact on reproductive medicine. for example, for embryos fertilized in vitro, researchers can trigger the dormancy of embryos by regulating mtor signaling, providing a longer window for assessing embryo health and ensuring the embryo’s health. survival and subsequent healthy development.[2] mTOR activity paces human blastocyst stage developmental progression. Cell (2024). DOI: 10.1016/j.cell.2024.08.048
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