Tissue-level cell tracking and analysis of actomyosin and N-cadherin adhesion dynamics, coupled with disruption of the regulatory gene Shroom3, reveals region-specific cell behaviors along the anteroposterior axis during neural tube closure.

Stem-cell-specific transcriptional repressors fine-tune levels of stemness gene transcripts in asymmetrically dividing neural stem cells by depositing low levels of repressive histone marks at these loci allowing progeny to rapidly initiate differentiation.

Closure of the cranial neural tube, which is essential for mammalian development, is driven by spatially and temporally patterned cell remodeling events that require positionally regulated Sonic hedgehog signaling.

Human neural tube closure defects associated mutations in planar cell polarity (PCP) genes are causative of the disease, as revealed in the intricate Drosophila PCP model.

Planar cell polarity proteins display dynamic spatial and temporal patterns of enrichment that tightly correlate with myosin-dependent cell behaviors during neural tube closure.

A fibronectin matrix constantly remodels to the area of highest mechanical stress, and the resulting fibronectin-mediated inter-tissue adhesion impedes neural tube convergence.

Analysis of 108 human embryos aged 3–7 weeks reveals modes of primary and secondary neurulation, regulation of body elongation, somite formation rate, and common occurrence of a split neural tube.

The completion of neural tube closure requires small GTPase-regulated membrane protrusions from non-neural ectoderm cells at the tips of the neural folds.

Neural tube-associated boundary caps are heterogeneous with a non-neural crest-derived subpopulation that may originate from the developing meninges, which gives rise to derivatives that migrate along nerves to detach and differentiate into skin mural cells.

The cell cycle phosphatase CDC25B controls cell cycle progression and neurogenesis through independent pathways.