Gabriel L. Galea

This study shows that ECM defects in Down syndrome neurodevelopment cause apical cytoarchitecture and mechanical property instability in neural stem cell models.

This study shows that local anisotropic stress and cytoskeletal organization, rather than actomyosin purse-string contraction, drive cell shape and motion during hindbrain neuropore closure in mouse embryos.

The paper demonstrates that Chiari II brain malformation arises secondary to open spina bifida in mice, showing structural brain and skull defects linked to neurogenesis and neuronal migration disturbances.

The paper shows that sparse mesenchymal networks behave like a fluid under tension, driven by contact inhibition of locomotion, and identifies this as a new tissue behavior with implications for development and tumorigenesis.

This study shows that CLDN3 depletion in chick embryos increases tissue tension, leading to neural fold fusion defects in the spinal region by altering apical cytoskeletal dynamics.

The paper identifies a lateral tension mechanism in murine neural tube closure distinct from contractile hinge mechanisms in other systems.

This study examines spinal neural tube formation and tail development in human embryos, finding patterns similar to mouse and rat, including primary neurulation completion and secondary neurulation characteristics.

This study identifies CFL1-dependent cell behaviours driving spinal zippering in mice and shows that its deletion impairs zippering and causes spina bifida.

This study shows that disrupting Fgfr1 in mice causes localized spinal mis-patterning and a terminal myelocystocele-like phenotype after neural tube closure.

The paper shows that severe neural tube defects can occur without abnormal convergent extension by linking GAG sulfation and partial PCP gene loss.

The paper shows that the geometry of the hindbrain neuropore in mouse embryos determines asymmetric closure dynamics through cell-mediated mechanisms.

This study identifies transient basal protrusions in zebrafish spinal neurons that regulate spatiotemporal differentiation patterns through lateral inhibition.

This paper introduces a novel mouse model of encephalocele showing it arises post-neurulation and can share genetic causes with anencephaly.