PUBLICATION
ECM alterations in Fndc3a (Fibronectin Domain Containing Protein 3A) deficient zebrafish cause temporal fin development and regeneration defects
- Authors
- Liedtke, D., Orth, M., Meissler, M., Geuer, S., Knaup, S., Köblitz, I., Klopocki, E.
- ID
- ZDB-PUB-190919-7
- Date
- 2019
- Source
- Scientific Reports 9: 13383 (Journal)
- Registered Authors
- Klopocki, Eva, Knaup, Sabine, Liedtke, Daniel
- Keywords
- none
- MeSH Terms
-
- Animal Fins/metabolism
- Animal Fins/pathology*
- Animals
- Extracellular Matrix/metabolism
- Extracellular Matrix/pathology*
- Gene Expression Regulation, Developmental*
- Protein Domains
- Regeneration*
- Wound Healing*
- Zebrafish/metabolism*
- Zebrafish Proteins/deficiency*
- PubMed
- 31527654 Full text @ Sci. Rep.
Citation
Liedtke, D., Orth, M., Meissler, M., Geuer, S., Knaup, S., Köblitz, I., Klopocki, E. (2019) ECM alterations in Fndc3a (Fibronectin Domain Containing Protein 3A) deficient zebrafish cause temporal fin development and regeneration defects. Scientific Reports. 9:13383.
Abstract
Fin development and regeneration are complex biological processes that are highly relevant in teleost fish. They share genetic factors, signaling pathways and cellular properties to coordinate formation of regularly shaped extremities. Especially correct tissue structure defined by extracellular matrix (ECM) formation is essential. Gene expression and protein localization studies demonstrated expression of fndc3a (fibronectin domain containing protein 3a) in both developing and regenerating caudal fins of zebrafish (Danio rerio). We established a hypomorphic fndc3a mutant line (fndc3awue1/wue1) via CRISPR/Cas9, exhibiting phenotypic malformations and changed gene expression patterns during early stages of median fin fold development. These developmental effects are mostly temporary, but result in a fraction of adults with permanent tail fin deformations. In addition, caudal fin regeneration in adult fndc3awue1/wue1 mutants is hampered by interference with actinotrichia formation and epidermal cell organization. Investigation of the ECM implies that loss of epidermal tissue structure is a common cause for both of the observed defects. Our results thereby provide a molecular link between these developmental processes and foreshadow Fndc3a as a novel temporal regulator of epidermal cell properties during extremity development and regeneration in zebrafish.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping