Nodal/Smad2 signaling maintains diapause in the mouse embryo.

Nodal/Smad2 signaling maintains embryonic diapause in mice by repressing lipid storage pathways in blastocysts.

• Why it matters: Understanding how diapause is regulated can reveal mechanisms of embryo survival under stress, which is crucial for reproductive biology and potential clinical applications.
• What they did: Furlan et al. used molecular analysis to show that Nodal/Smad2 signaling suppresses Pparg-driven lipid accumulation, thereby sustaining the dormant state in mouse blastocysts.
• The result: This discovery highlights a key signaling pathway that controls embryo dormancy, offering insights into developmental regulation and potential targets for fertility interventions.