Endocardial cells in the valve-forming region undergo a significant volume reduction during early heart development.
⚖️ Piezo1 fine-tunes this process through a dual mechanism: in the short term, promoting membrane trafficking of Aqp8a.1 for rapid cell volume adjustment, and in the long term, suppressing aqp8a.1 transcription via Notch1b signaling to prevent excessive shrinkage.
💡 Together, our findings reveal that mechanotransduction can dictate organ formation through the dynamic regulation of cell volume, uncovering a fundamental principle of morphogenesis.
💧 In response to mechanical stimulation and calmodulin activation, Aqp8a.1 is incorporated into the plasma membrane, enabling cell volume loss that drives heart looping and valve formation.
Here, we show that:
🔬 The mechanosensitive ion channel Piezo1 works together with calmodulin and the aquaporin water channel Aqp8a.1 to orchestrate endocardial cell shrinkage.
A huge thank you to all our fantastic collaborators (@kkalyviotis.bsky.social, Shuyi Feng, Antoine Sanchez, Igor Kondrychyn, Moe Fukumoto, Xiangbin Pan, Thomas Juan, @stainierlab.bsky.social, @pantazislab.bsky.social, @phnglab.bsky.social) and @imperialcollegeldn.bsky.social!
🚨 How do mechanical forces shape a developing organ?
Our new #ScienceAdvances @science.org study, led by the amazing @cvagenapantoula.bsky.social, reveals a Piezo1-driven hydraulic mechanism, where mechanical cues control cell volume to guide cardiac formation ❤️🐟
🔗 www.science.org/doi/10.1126/...
Check out our latest preprint on the cellular mechanical basis of Voronoi tessellations in epithelia! This biophysics study is inspired by disordered tessellations observed in zebrafish hearts 🤓🐟💙 #SulaimaanLim #ChiuFanLeeLab
arxiv.org/html/2512.13...
🧠 Join us @uzh-ch.bsky.social ! We are a new lab looking for PhDs, Postdocs & Master’s students interested in studying how human neural systems emerge & go awry using brain organoids, light-sheet imaging & genomics. 🚀 Deadline for LSZGS 1st Nov! www.lifescience-graduateschool.uzh.ch/en.html.