Increased tissue tension caused by depletion of CLDN3 in the non-neural ectoderm causes neural tube defects in chick embryos.

Authors

Elizabeth-Ann Legere, Marie Dumont, Jordan Dias, Yojiro Yamanaka, Gabriel L Galea, Aimee K Ryan

Published in

Journal of cell science. Aug 17, 2026. Epub Aug 17, 2026.

Abstract

Neural tube morphogenesis provides a dynamic setting to study epithelial cell behaviours. Here, we examined CLDN3-dependent biomechanical properties of the non-neural ectoderm during neural tube closure in chick embryos. Previous analyses of static images of chick embryos suggested that spinal neural tube closure occurs through multiple contact points or "buttoning". Using live imaging and transverse cuts through the neural folds we confirmed the multiple simultaneous "buttoning" contacts along the anterior-posterior axis and showed that spinal neural fold fusion is not the result of progressive "zippering" cell behaviors required in cranial and posterior neuropore regions. CLDN3-depletion decreased the rate of neural fold closure between points of contact and increased pMLC within the apical domain of non-neural ectoderm cells suggesting increased actomyosin contraction. Laser ablation studies revealed that CLDN3-depleted embryos exhibited higher tension across the non-neural ectoderm during neural fold fusion. Decreasing tension with blebbistatin rescued the neural fold fusion defects in CLDN3-depleted embryos. Our data support the importance of CLDN3 to regulate tissue tension through effects on cytoskeletal dynamics in the non-neural ectoderm during neural fold fusion.

PMID:
42605241
Bibliographic data and abstract were imported from PubMed on 17 Aug 2026.

Read full publication at:
Please sign in to see all details.

Stats

1-terrible, 9-excellent. How would you rate this publication? Sign in in to submit your rating.

Post a comment

You need to be signed in to post comments. You can sign in here.

Comments

There are no comments yet.