PUBLICATION
Specific CaMKIIs mediate convergent extension cell movements in early zebrafish development
- Authors
- McLeod, J.J., Rothschild, S.C., Francescatto, L., Kim, H., Tombes, R.M.
- ID
- ZDB-PUB-231020-63
- Date
- 2023
- Source
- Developmental Dynamics : an official publication of the American Association of Anatomists 253(4): 390-403 (Journal)
- Registered Authors
- Francescatto, Ludmila, McLeod, Jamie, Rothschild, Sarah Chase, Tombes, Robert M.
- Keywords
- CaMKII, Wnt11, calcium, convergent extension, gastrulation, midline bifurcation, zebrafish
- MeSH Terms
-
- Animals
- Calcium-Calmodulin-Dependent Protein Kinase Type 2/genetics
- Cell Movement/physiology
- Gastrulation/physiology
- Zebrafish*/genetics
- Zebrafish Proteins*/genetics
- Zebrafish Proteins*/metabolism
- PubMed
- 37860955 Full text @ Dev. Dyn.
Citation
McLeod, J.J., Rothschild, S.C., Francescatto, L., Kim, H., Tombes, R.M. (2023) Specific CaMKIIs mediate convergent extension cell movements in early zebrafish development. Developmental Dynamics : an official publication of the American Association of Anatomists. 253(4):390-403.
Abstract
Background Noncanonical Wnts are morphogens that can elevate intracellular Ca2+ , activate the Ca2+ /calmodulin-dependent protein kinase, CaMKII, and promote cell movements during vertebrate gastrulation.
Results Zebrafish express seven CaMKII genes during embryogenesis; two of these, camk2b1 and camk2g1, are necessary for convergent extension (CE) cell movements. CaMKII morphant phenotypes were observed as early as epiboly. At the 1-3 somite stage, neuroectoderm and paraxial cells remained unconverged in both morphants. Later, somites lacked their stereotypical shape and were wider, more closely spaced, and body gap angles increased. At 24hpf, somite compression and notochord undulation coincided with a shorter and broader body axis. A camk2b1 crispant was generated which phenocopied the camk2b1 morphant. The levels of cell proliferation, apoptosis and paraxial and neuroectodermal markers were unchanged in morphants. Hyperactivation of CaMKII during gastrulation by transient pharmacological intervention (thapsigargin) also caused CE defects. Mosaically expressed dominant-negative CaMKII recapitulated these phenotypes and showed significant midline bifurcation. Finally, the introduction of CaMKII partially rescued Wnt11 morphant phenotypes.
Conclusions Overall, these data support a model whereby cyclically activated CaMKII encoded from two genes enables cell migration during the process of CE.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping