PUBLICATION
Lef1 controls patterning and proliferation in the posterior lateral line system of zebrafish
- Authors
- Gamba, L., Cubedo, N., Lutfalla, G., Ghysen, A., and Dambly-Chaudiere, C.
- ID
- ZDB-PUB-101101-14
- Date
- 2010
- Source
- Developmental Dynamics : an official publication of the American Association of Anatomists 239(12): 3163-3171 (Journal)
- Registered Authors
- Cubedo, Nicolas, Ghysen, Alain, Lutfalla, Georges
- Keywords
- PLL, neuromast, primordium, cxcr4, cxcr7, Wnt
- MeSH Terms
-
- Animals
- Body Patterning/genetics
- Body Patterning/physiology*
- Cell Proliferation
- In Situ Hybridization
- Lateral Line System/embryology*
- Polymerase Chain Reaction
- Promoter Regions, Genetic/genetics
- Receptors, CXCR/genetics
- Receptors, CXCR4/genetics
- Transcription Factors/genetics
- Transcription Factors/metabolism*
- Zebrafish
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- PubMed
- 20981829 Full text @ Dev. Dyn.
Citation
Gamba, L., Cubedo, N., Lutfalla, G., Ghysen, A., and Dambly-Chaudiere, C. (2010) Lef1 controls patterning and proliferation in the posterior lateral line system of zebrafish. Developmental Dynamics : an official publication of the American Association of Anatomists. 239(12):3163-3171.
Abstract
The embryonic development of the posterior lateral line of zebrafish involves the migration from head to tail of a primordium comprising approximately 100 cells, and the deposition at regular intervals of presumptive mechanosensory organs (neuromasts). Migration depends on the presence of chemokine SDF1 along the pathway, and on the asymmetrical distribution of chemokine receptors CXCR4 and CXCR7 in the primordium. Primordium polarization depends on Wnt signaling in the leading region. Here, we examine the role of a major effector of Wnt signaling, lef1, in this system. We show that, although its inactivation has no overt effect on the expression of cxcr4b and cxcr7b, lef1 contributes to their control. We also show that cell proliferation, which ensures constant primordium size despite successive rounds of cell deposition, is reduced upon lef1 inactivation. Because of this defect, the primordium runs short of cells and vanishes before the line has been completed. We conclude that lef1-mediated Wnt signaling is involved in various aspects of primordium migration, although part of this implication is masked by a high level of developmental redundancy.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping