PUBLICATION
An essential role for parathyroid hormone in gill formation and differentiation of ion-transporting cells in developing zebrafish
- Authors
- Kwong, R.W., Perry, S.F.
- ID
- ZDB-PUB-150415-2
- Date
- 2015
- Source
- Endocrinology 156(7): 2384-94 (Journal)
- Registered Authors
- Keywords
- none
- MeSH Terms
-
- Animals
- Branchial Region/growth & development
- Branchial Region/metabolism
- Cartilage/growth & development*
- Cartilage/metabolism
- Cell Differentiation
- Chondrocytes/cytology
- Chondrocytes/metabolism
- DNA-Binding Proteins/genetics*
- Epithelial Cells/cytology
- Epithelial Cells/metabolism
- Gene Expression Regulation, Developmental/genetics*
- Gene Knockdown Techniques
- Gills/growth & development*
- Gills/metabolism
- Larva
- Parathyroid Hormone/metabolism*
- Proton-Translocating ATPases/metabolism
- RNA, Messenger/metabolism*
- Real-Time Polymerase Chain Reaction
- Sodium-Potassium-Exchanging ATPase/metabolism
- TRPV Cation Channels/metabolism
- Transcription Factors/genetics*
- Zebrafish
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- PubMed
- 25872007 Full text @ Endocrinology
Citation
Kwong, R.W., Perry, S.F. (2015) An essential role for parathyroid hormone in gill formation and differentiation of ion-transporting cells in developing zebrafish. Endocrinology. 156(7):2384-94.
Abstract
In vertebrates, parathyroid hormone (PTH) is important for skeletogenesis and Ca(2+) homeostasis. However, little is known about the molecular mechanisms by which PTH regulates skeleton formation and Ca(2+) balance during early development. Using larval zebrafish as an in vivo model system, we determined that PTH1 regulates the differentiation of epithelial cells and the development of craniofacial cartilage. We demonstrated that translational gene knockdown of PTH1 decreased Ca(2+) uptake at 4 days post fertilization (dpf). We also observed that PTH1-deficient fish exhibited reduced numbers of epithelial Ca(2+) channel (ecac)-expressing cells, Na(+)/K(+)-ATPase-rich cells and H(+)-ATPase-rich cells. Additionally, the density of epidermal stem cells was decreased substantially in fish experiencing PTH1 knockdown. Knockdown of PTH1 caused a shortening of the jaw and impeded the development of branchial arches. Results from in situ hybridization suggested that expression of collagen2a1a (marker for proliferating chondrocytes) was substantially reduced in the cartilage that forms the jaw and branchial aches. Disorganization of chondrocytes in craniofacial cartilage also was observed in PTH1-deficient fish. The results of real-time PCR demonstrated that PTH1 morphants failed to express the transcription factor glial cell missing 2 (gcm2). Co-injection of PTH1 morpholino with gcm2 cRNA rescued the phenotypes observed in the PTH1 morphants, suggesting that the defects in PTH1-deficient fish were caused, at least in part, by the suppression of gcm2. Taken together, the results of the present study reveal critical roles for PTH1 in promoting the differentiation of epidermal stem cells into mature ionocytes and cartilage formation during development.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping