期刊
出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.2100500118
关键词
embryonic diapause; European roe deer (Capreolus capreolus); embryo development
资金
- European Cooperation in Science and Technology Action [CA16119]
- Swiss NSF [31003A_159734, 310030_ 185026]
- Swiss National Science Foundation (SNF) [31003A_159734, 310030_185026] Funding Source: Swiss National Science Foundation (SNF)
Embryonic diapause in mammals leads to reversible developmental arrest, with European roe deer embryos showing continuous deceleration. The role of maternal-origin amino acids in driving embryonic developmental pace is proposed, with potential involvement of mTORC1 and mTORC2 in regulating proliferation rate during diapause.
Embryonic diapause in mammals leads to a reversible developmental arrest. While completely halted in many species, European roe deer (Capreolus capreolus) embryos display a continuous deceleration of proliferation. During a 4-mo period, the cell doubling time is 2 to 3 wk. During this period, the preimplantation blastocyst reaches a diameter of 4 mm, after which it resumes a fast developmental pace to subsequently implant. The mechanisms regulating this notable deceleration and reacceleration upon developmental resumption are unclear. We propose that amino acids of maternal origin drive the embryonic developmental pace. A pronounced change in the abundance of uterine fluid mTORC1-activating amino acids coincided with an increase in embryonic mTORC1 activity prior to the resumption of development. Concurrently, genes related to the gly-colytic and phosphate pentose pathway, the TCA cycle, and one carbon metabolism were up-regulated. Furthermore, the uterine luminal epithelial transcriptome indicated increased estradiol-17 beta signaling, which likely regulates the endometrial secretions adapting to the embryonic needs. While mTORC1 was predicted to be inactive during diapause, the residual embryonic mTORC2 activity may indicate its involvement in maintaining the low yet continuous proliferation rate during diapause. Collectively, we emphasize the role of nutrient signaling in preimplantation embryo development. We propose selective mTORC1 inhibition via uterine catecholestrogens and let-7 as a mechanism regulating slow stem cell cycle progression.
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