Nodal/Smad2 signaling sustains developmental pausing by repressing Pparg-mediated lipid metabolism.
Nodal/Smad2 signaling is essential for maintaining embryonic diapause by repressing Pparg-mediated lipid metabolism, preventing lipid accumulation during dormancy.
- Why it matters: Understanding how active signaling pathways sustain dormancy can reveal mechanisms controlling developmental pauses and related conditions like cancer dormancy and metabolic disorders.
- What they did: The study examined Nodal/Smad2 pathway activation during diapause in vivo and used ex vivo blastocyst and embryonic stem cell models to investigate its role in repressing Pparg, a key regulator of lipid storage.
- The result: Disruption of Smad2-mediated Pparg repression causes lipid buildup and impairs diapause, highlighting a crucial Nodal-Smad2-Pparg axis that maintains the metabolic state necessary for developmental dormancy.