PUBLICATION
Calcium signals drive cell shape changes during zebrafish midbrain-hindbrain boundary formation
- Authors
- Sahu, S.U., Visetsouk, M.R., Garde, R.J., Hennes, L., Kwas, C., Gutzman, J.H.
- ID
- ZDB-PUB-170204-10
- Date
- 2017
- Source
- Molecular biology of the cell 28(7): 875-882 (Journal)
- Registered Authors
- Gutzman, Jennifer, Kwas, Connie, Sahu, Srishti, Visetsouk, Mike
- Keywords
- none
- MeSH Terms
-
- Animals
- Brain/embryology
- Brain/metabolism
- Calcium/metabolism*
- Cell Shape/genetics
- Cell Shape/physiology*
- Embryonic Development
- Gene Expression Regulation, Developmental/genetics
- Mesencephalon/embryology
- Mesencephalon/metabolism
- Molecular Motor Proteins/metabolism
- Morphogenesis
- Myosin Type II/metabolism*
- Organogenesis
- Phosphorylation
- Rhombencephalon/embryology
- Rhombencephalon/metabolism
- Signal Transduction
- Zebrafish/genetics
- Zebrafish/metabolism
- Zebrafish/physiology
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism
- PubMed
- 28148652 Full text @ Mol. Biol. Cell
Citation
Sahu, S.U., Visetsouk, M.R., Garde, R.J., Hennes, L., Kwas, C., Gutzman, J.H. (2017) Calcium signals drive cell shape changes during zebrafish midbrain-hindbrain boundary formation. Molecular biology of the cell. 28(7):875-882.
Abstract
One of the first morphogenetic events in the vertebrate brain is the formation of the highly conserved midbrain-hindbrain boundary (MHB). Specific cell shape changes occur at the point of deepest constriction of the MHB, the midbrain-hindbrain boundary constriction (MHBC), and are critical for proper MHB formation. These cell shape changes are controlled by nonmuscle myosin II (NMII) motor proteins, which are tightly regulated via the phosphorylation of their associated myosin regulatory light chains (MRLCs). However, the upstream signaling pathways that initiate the regulation of NMII to mediate cell shape changes during MHB morphogenesis are not known. We show that intracellular calcium signals are critical for the regulation of cell shortening during initial MHB formation. We demonstrate that the MHB region is poised to respond to calcium transients that occur in the MHB at the onset of MHB morphogenesis and that calcium mediates phosphorylation of MRLC specifically in MHB tissue. Our results indicate that calmodulin 1a (calm1a), expressed specifically in the MHB, and myosin light chain kinase together mediate MHBC cell length. Our data suggest that modulation of NMII activity by calcium is critical for proper regulation of cell length to determine embryonic brain shape during development.
Genes / Markers
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Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
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