Formation of the zebrafish midbrain-hindbrain boundary constriction requires laminin-dependent basal constriction
- Gutzman, J.H., Graeden, E.G., Lowery, L.A., Holley, H.S., and Sive, H.
- Mechanisms of Development 125(11-12): 974-983 (Journal)
- Registered Authors
- Gutzman, Jennifer, Lowery, Laura Anne, Sive, Hazel
- basal constriction, apical expansion, zebrafish morphogenesis, laminin, brain ventricle, midbrain-hindbrain boundary, midbrain-hindbrain boundary constriction (MHBC), cell shape
- MeSH Terms
- Cell Shape
- Cell Size
- Models, Biological
- Neural Crest/metabolism
- 18682291 Full text @ Mech. Dev.
Gutzman, J.H., Graeden, E.G., Lowery, L.A., Holley, H.S., and Sive, H. (2008) Formation of the zebrafish midbrain-hindbrain boundary constriction requires laminin-dependent basal constriction. Mechanisms of Development. 125(11-12):974-983.
The midbrain-hindbrain boundary (MHB) is a highly conserved fold in the vertebrate embryonic brain. We have termed the deepest point of this fold the MHB constriction (MHBC) and have begun to define the mechanisms by which it develops. In the zebrafish, the MHBC is formed soon after neural tube closure, concomitant with inflation of the brain ventricles. The MHBC is unusual, as it forms by bending the basal side of the neuroepithelium. At single cell resolution, we show that zebrafish MHBC formation involves two steps. The first is a shortening of MHB cells to approximately 75% of the length of surrounding cells. The second is basal constriction, and apical expansion, of a small group of cells that contribute to the MHBC. In the absence of inflated brain ventricles, basal constriction still occurs, indicating that the MHBC is not formed as a passive consequence of ventricle inflation. In laminin mutants, basal constriction does not occur, indicating an active role for the basement membrane in this process. Apical expansion also fails to occur in laminin mutants, suggesting that apical expansion may be dependent on basal constriction. This study demonstrates laminin-dependent basal constriction as a previously undescribed molecular mechanism for brain morphogenesis.
Genes / Markers
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Engineered Foreign Genes
Errata and Notes