PUBLICATION
Lgl2 and E-cadherin act antagonistically to regulate hemidesmosome formation during epidermal development in zebrafish
- Authors
- Sonawane, M., Martin-Maischein, H., Schwarz, H., and Nüsslein-Volhard, C.
- ID
- ZDB-PUB-090310-9
- Date
- 2009
- Source
- Development (Cambridge, England) 136(8): 1231-1240 (Journal)
- Registered Authors
- Nüsslein-Volhard, Christiane, Sonawane, Mahendra
- Keywords
- Lgl2 (Llgl2), E-cadherin (Cadherin 1), Hemidesmosome formation, Epidermis, Zebrafish
- MeSH Terms
-
- Animals
- Cadherins/metabolism*
- Cell Differentiation
- Cell Membrane/metabolism
- Epidermis/cytology
- Epidermis/growth & development*
- Epidermis/metabolism*
- Gene Expression Regulation, Developmental
- Hemidesmosomes/genetics
- Hemidesmosomes/metabolism*
- Integrin alpha6/metabolism
- Isoenzymes/metabolism
- Microscopy, Immunoelectron
- Protein Kinase C/metabolism
- Zebrafish/genetics
- Zebrafish/growth & development*
- Zebrafish/metabolism*
- beta Karyopherins/genetics
- beta Karyopherins/metabolism*
- PubMed
- 19261700 Full text @ Development
Citation
Sonawane, M., Martin-Maischein, H., Schwarz, H., and Nüsslein-Volhard, C. (2009) Lgl2 and E-cadherin act antagonistically to regulate hemidesmosome formation during epidermal development in zebrafish. Development (Cambridge, England). 136(8):1231-1240.
Abstract
The integrity and homeostasis of the vertebrate epidermis depend on various cellular junctions. How these junctions are assembled during development and how their number is regulated remain largely unclear. Here, we address these issues by analysing the function of Lgl2, E-cadherin and atypical Protein kinase C (aPKC) in the formation of hemidesmosomes in the developing basal epidermis of zebrafish larvae. Previously, we have shown that a mutation in lgl2 (penner) prevents the formation of hemidesmosomes. Here we show that Lgl2 function is essential for mediating the targeting of Integrin alpha 6 (Itga6), a hemidesmosomal component, to the plasma membrane of basal epidermal cells. In addition, we show that whereas aPKClambda seems dispensable for the localisation of Itga6 during hemidesmosome formation, knockdown of E-cadherin function leads to an Lgl2-dependent increase in the localisation of Itga6. Thus, Lgl2 and E-cadherin act antagonistically to control the localisation of Itga6 during the formation of hemidesmosomes in the developing epidermis.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping