Cellular basis of neuroepithelial bending during mouse spinal neural tube closure.
Bottom Line: As the neural folds elevate, cell numbers increase to a greater extent in the dorsolateral neural plate that contacts the surface ectoderm, compared with the more ventromedial neural plate where cells contact paraxial mesoderm and notochord.The translocation of cells into the neural fold, together with its more rapid cell proliferation, leads to an increase in cell density dorsolaterally compared with the more ventromedial neural plate.These findings suggest a model in which DLHP formation may proceed through 'buckling' of the neuroepithelium at a dorso-ventral boundary marked by a change in cell-packing density.
Affiliation: Newlife Birth Defects Research Centre, Institute of Child Health, University College London, 30 Guilford Street, London WC1N 1EH, UK.Show MeSH
Mentions: It is striking that DLHPs form precisely at the dorso-ventral level where the neural plate transitions from basal contact with paraxial mesoderm to basal contact with surface ectoderm. We found that, during DLHP formation, both cell number and cell density increase markedly, while nominal cell width decreases, particularly in the dorsal neural fold component of the neuroepithelium. This might suggest a mechanism of neural plate bending (Fig. 8) in which the elevating neuroepithelium behaves biomechanically as a biphasic structure. That is, each half-neural plate comprises a dorsolateral component of increasing cell density in direct physical contiguity with a ventromedial component of relatively constant, lower cell density. We suggest, therefore, that DLHP formation could represent the inward (i.e. medially directed) ‘buckling’ of the neuroepithelium at the phase transition point (see red arrow: ‘basal contact transition point’ in Fig. 8). This represents a markedly different view of neuroepithelial morphogenesis from the rather uniform bending that is usually envisaged to result from generalised apical constriction of the neuroepithelium (Sawyer et al., 2010).
Affiliation: Newlife Birth Defects Research Centre, Institute of Child Health, University College London, 30 Guilford Street, London WC1N 1EH, UK.