PUBLICATION
Intracellular Calcium Mobilization Is Required for Sonic Hedgehog Signaling
- Authors
- Klatt Shaw, D., Gunther, D., Jurynec, M.J., Chagovetz, A.A., Ritchie, E., Grunwald, D.J.
- ID
- ZDB-PUB-180515-2
- Date
- 2018
- Source
- Developmental Cell 45(4): 512-525.e5 (Journal)
- Registered Authors
- Grunwald, David, Jurynec, Michael
- Keywords
- hedgehog signaling, intracellular calcium release, ryanodine receptors, tissue pattering
- MeSH Terms
-
- Animals
- Body Patterning
- Calcium/metabolism*
- Embryo, Nonmammalian/cytology
- Embryo, Nonmammalian/physiology*
- Gene Expression Regulation, Developmental*
- Hedgehog Proteins/genetics
- Hedgehog Proteins/metabolism*
- Morphogenesis
- Muscles/cytology
- Muscles/metabolism
- Neural Tube/cytology
- Neural Tube/metabolism
- Signal Transduction*
- Somites/cytology
- Somites/metabolism*
- Zebrafish/embryology
- Zebrafish/physiology*
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism
- PubMed
- 29754802 Full text @ Dev. Cell
Citation
Klatt Shaw, D., Gunther, D., Jurynec, M.J., Chagovetz, A.A., Ritchie, E., Grunwald, D.J. (2018) Intracellular Calcium Mobilization Is Required for Sonic Hedgehog Signaling. Developmental Cell. 45(4):512-525.e5.
Abstract
Graded Shh signaling across fields of precursor cells coordinates patterns of gene expression, differentiation, and morphogenetic behavior as precursors form complex structures, such as the nervous system, the limbs, and craniofacial skeleton. Here we discover that intracellular calcium mobilization, a process tightly controlled and readily modulated, regulates the level of Shh-dependent gene expression in responding cells and affects the development of all Shh-dependent cell types in the zebrafish embryo. Reduced expression or modified activity of ryanodine receptor (RyR) intracellular calcium release channels shifted the allocation of Shh-dependent cell fates in the somitic muscle and neural tube. Mosaic analysis revealed that RyR-mediated calcium mobilization is required specifically in Shh ligand-receiving cells. This work reveals that RyR channels participate in intercellular signal transduction events. As modulation of RyR activity modifies tissue patterning, we hypothesize that alterations in intracellular calcium mobilization contribute to both birth defects and evolutionary modifications of morphology.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping