PUBLICATION
Ff1b is required for the development of steroidogenic component of the zebrafish interrenal organ
- Authors
- Chai, C., Liu, Y., and Chan, W.K.
- ID
- ZDB-PUB-030730-7
- Date
- 2003
- Source
- Developmental Biology 260(1): 226-244 (Journal)
- Registered Authors
- Chan, Woon-Khiong, Liu, Yi-wen
- Keywords
- none
- MeSH Terms
-
- Aminoglutethimide/pharmacology
- Animals
- Body Patterning
- Cell Movement
- Cholesterol Side-Chain Cleavage Enzyme/genetics
- Cholesterol Side-Chain Cleavage Enzyme/metabolism
- Embryo, Nonmammalian
- Enzyme Inhibitors/pharmacology
- Gene Expression Regulation, Developmental
- Interrenal Gland/drug effects
- Interrenal Gland/growth & development*
- Interrenal Gland/physiology
- Mutation
- Oligonucleotides, Antisense/pharmacology
- Recombinant Fusion Proteins/metabolism
- Trans-Activators/metabolism
- Transcriptional Activation
- Water-Electrolyte Balance/drug effects
- Zebrafish/embryology*
- Zebrafish Proteins/drug effects
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- PubMed
- 12885566 Full text @ Dev. Biol.
Citation
Chai, C., Liu, Y., and Chan, W.K. (2003) Ff1b is required for the development of steroidogenic component of the zebrafish interrenal organ. Developmental Biology. 260(1):226-244.
Abstract
The zebrafish ftz-f1 gene, ff1b, is activated in two cell clusters lateral to the midline in the trunk during late embryogenesis. These cell clusters coalesce to form a discrete organ at around 30 hpf, which then begins to acquire a steroidogenic identity as evidenced by the expression of the steroidogenic enzyme genes, cyp11a and 3beta-hsd. The migration of the cell clusters to the midline is impaired in zebrafish midline signaling mutants. Knockdown of Ff1b activity by antisense ff1b morpholino oligonucleotide (ff1bMO) leads to phenotypes that are consistent with impaired osmoregulation. Injection of ff1bMO was also shown to downregulate the expression of cyp11a and 3beta-hsd. Histological comparison of wild-type and ff1b morphants at various embryonic and juvenile stages revealed the absence of interrenal tissue development in ff1b morphants. The morphological defects of ff1b morphants could be mimicked by treatment with aminoglutethimide, an inhibitor of de novo steroid synthesis. Based on these data, we propose that ff1b is required for the development of the steroidogenic tissue of the interrenal organ.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping