PUBLICATION
Redundant roles of PRDM family members in zebrafish craniofacial development
- Authors
- Ding, H.L., Clouthier, D.E., and Artinger, K.B.
- ID
- ZDB-PUB-121120-12
- Date
- 2013
- Source
- Developmental Dynamics : an official publication of the American Association of Anatomists 242(1): 67-79 (Journal)
- Registered Authors
- Artinger, Kristin Bruk, Ding, Hailei
- Keywords
- prdm, craniofacial development, neural crest cell, zebrafish, mopholino, dlx2a, barx1
- MeSH Terms
-
- Animals
- DNA Primers/genetics
- Face/embryology*
- Gene Expression Regulation, Developmental/genetics*
- Genotype
- Image Processing, Computer-Assisted
- In Situ Hybridization
- Morpholinos/genetics
- Multigene Family/genetics*
- Neural Crest/cytology
- Neural Crest/metabolism
- Skull/embryology*
- Transcription Factors/genetics
- Transcription Factors/metabolism*
- Tumor Suppressor Proteins/genetics
- Tumor Suppressor Proteins/metabolism*
- Zebrafish/embryology*
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- PubMed
- 23109401 Full text @ Dev. Dyn.
Citation
Ding, H.L., Clouthier, D.E., and Artinger, K.B. (2013) Redundant roles of PRDM family members in zebrafish craniofacial development. Developmental Dynamics : an official publication of the American Association of Anatomists. 242(1):67-79.
Abstract
Background: PRDM proteins are evolutionary conserved Zn-Finger transcription factors that share a characteristic protein domain organization. Previous studies have shown that prdm1a is required for the specification and differentiation of neural crest cells in the zebrafish. Results: Here we examine other members of this family, specifically prdm3, 5, and 16, in the differentiation of the zebrafish craniofacial skeleton. prdm3 and prdm16 are strongly expressed in the pharyngeal arches, while prdm5 is expressed specifically in the area of the forming neurocranium. Knockdown of prdm3 and prdm16 results in a reduction in the neural crest markers dlx2a and barx1 and defects in both the viscerocranium and the neurocranium. The knockdown of prdm3 and prdm16 in combination is additive in the neurocranium, but not in the viscerocranium. Injection of sub-optimal doses of prdm1a with prdm3 or prdm16 Morpholinos together leads to more severe phenotypes in the viscerocranium and neurocranium. prdm5 mutants have defects in the neurocranium and prdm1a and prdm5 double mutants also show more severe phenotypes. Conclusions: Overall, our data reveal that prdm3, 5, and 16 are involved in the zebrafish craniofacial development and that prdm1a may interact with prdm3, 5, and 16 in the formation of the craniofacial skeleton in zebrafish.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping