Some mammals pause pregnancy through embryonic diapause, but humans are an exception. A study published in Genes & Development explains how diapaused embryonic stem cells from mice retain pluripotency during long periods of low metabolism or missing growth signals.
Earlier work showed several routes into a diapause-like state: blocking mTOR, reducing Myc transcription factors, or changing chromatin regulators such as MOF. In the new experiments the team used the BET inhibitor I-BET151 to mimic Myc loss and used mTOR inhibition to mimic nutrient scarcity. In both cases murine embryonic stem cells sharply reduced metabolism, RNA production and protein synthesis while remaining able to form many cell types.
All stressors activated the same response: genes that act as brakes on the MAP kinase pathway switched on. Different stresses displaced a protein called Capicua, which normally keeps those brake genes silent; removing Capicua allowed the brakes to engage and preserve pluripotency. The authors suggest this shared switch helps explain how various cells survive long metabolic stress.
Difficult words
- pluripotency — Ability of a cell to become many types
- embryonic stem cell — An early cell that can make body tissuesembryonic stem cells
- metabolism — All chemical processes that keep cells active
- inhibitor — A substance that slows or stops activity
- transcription factor — A protein that controls gene activityMyc transcription factors
- chromatin regulator — A protein that changes DNA packagingchromatin regulators
- stressor — Something that causes pressure or difficulty for cellsstressors
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Discussion questions
- How might understanding this shared switch help medical research or new therapies?
- Why do you think humans are an exception to embryonic diapause?
- Can you give an example of an animal or situation where lowering metabolism helps survival?
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