PUBLICATION
Zygotic vinculin is not essential for embryonic development in zebrafish
- Authors
- Han, M.K.L., van der Krogt, G.N.M., de Rooij, J.
- ID
- ZDB-PUB-170803-1
- Date
- 2017
- Source
- PLoS One 12: e0182278 (Journal)
- Registered Authors
- Keywords
- Zebrafish, Embryos, TALENs, Edema, Vertebrates, Sequence alignment, Multiple alignment calculation, Skeletal muscles
- MeSH Terms
-
- Animals
- Cell Adhesion
- Dogs
- Embryonic Development
- Extracellular Matrix/metabolism
- Gene Expression Regulation, Developmental
- Gene Knockout Techniques
- HEK293 Cells
- Humans
- Madin Darby Canine Kidney Cells
- Mechanotransduction, Cellular
- Vinculin/genetics*
- Vinculin/metabolism*
- Zebrafish/genetics
- Zebrafish/growth & development*
- Zebrafish/metabolism
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism
- PubMed
- 28767718 Full text @ PLoS One
Citation
Han, M.K.L., van der Krogt, G.N.M., de Rooij, J. (2017) Zygotic vinculin is not essential for embryonic development in zebrafish. PLoS One. 12:e0182278.
Abstract
The formation of multicellular tissues during development is governed by mechanical forces that drive cell shape and tissue architecture. Protein complexes at sites of adhesion to the extracellular matrix (ECM) and cell neighbors, not only transmit these mechanical forces, but also allow cells to respond to changes in force by inducing biochemical feedback pathways. Such force-induced signaling processes are termed mechanotransduction. Vinculin is a central protein in mechanotransduction that in both integrin-mediated cell-ECM and cadherin-mediated cell-cell adhesions mediates force-induced cytoskeletal remodeling and adhesion strengthening. Vinculin was found to be important for the integrity and remodeling of epithelial tissues in cell culture models and could therefore be expected to be of broad importance in epithelial morphogenesis in vivo. Besides a function in mouse heart development, however, the importance of vinculin in morphogenesis of other vertebrate tissues has remained unclear. To investigate this further, we knocked out vinculin functioning in zebrafish, which contain two fully functional isoforms designated as vinculin A and vinculin B that both show high sequence conservation with higher vertebrates. Using TALEN and CRISPR-Cas gene editing technology we generated vinculin-deficient zebrafish. While single vinculin A mutants are viable and able to reproduce, additional loss of zygotic vinculin B was lethal after embryonic stages. Remarkably, vinculin-deficient embryos do not show major developmental defects, apart from mild pericardial edemas. These results lead to the conclusion that vinculin is not of broad importance for the development and morphogenesis of zebrafish tissues.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping