PUBLICATION
miR-27 regulates chondrogenesis by suppressing Focal Adhesion Kinase during pharyngeal arch development
- Authors
- Kara, N., Wei, C., Commanday, A.C., Patton, J.G.
- ID
- ZDB-PUB-170621-12
- Date
- 2017
- Source
- Developmental Biology 429(1): 321-334 (Journal)
- Registered Authors
- Patton, James G.
- Keywords
- chondrogenesis, focal adhesion kinase, miR-27, pharyngeal arches, zebrafish
- MeSH Terms
-
- Animal Fins/embryology
- Animal Fins/metabolism
- Animals
- Branchial Region/embryology*
- Branchial Region/enzymology*
- Cartilage/pathology
- Cell Differentiation/genetics
- Cell Proliferation/genetics
- Cell Survival/genetics
- Chondrogenesis/genetics*
- Embryo, Nonmammalian/cytology
- Embryo, Nonmammalian/metabolism
- Focal Adhesion Protein-Tyrosine Kinases/metabolism*
- Gene Expression Regulation, Developmental
- Gene Knockdown Techniques
- MicroRNAs/genetics
- MicroRNAs/metabolism*
- Morphogenesis/genetics
- Neural Crest/cytology
- Zebrafish/embryology*
- Zebrafish/genetics*
- PubMed
- 28625871 Full text @ Dev. Biol.
Citation
Kara, N., Wei, C., Commanday, A.C., Patton, J.G. (2017) miR-27 regulates chondrogenesis by suppressing Focal Adhesion Kinase during pharyngeal arch development. Developmental Biology. 429(1):321-334.
Abstract
Cranial neural crest cells are a multipotent cell population that generate all the elements of the pharyngeal cartilage with differentiation into chondrocytes tightly regulated by temporal intracellular and extracellular cues. Here, we demonstrate a novel role for miR-27, a highly enriched microRNA in the pharyngeal arches, as a positive regulator of chondrogenesis. Knock down of miR-27 led to nearly complete loss of pharyngeal cartilage by attenuating proliferation and blocking differentiation of pre-chondrogenic cells. Focal adhesion kinase (FAK) is a key regulator in integrin-mediated extracellular matrix (ECM) adhesion and has been proposed to function as a negative regulator of chondrogenesis. We show that FAK is downregulated in the pharyngeal arches during chondrogenesis and is a direct target of miR-27. Suppressing the accumulation of FAK in miR-27 morphants partially rescued the severe pharyngeal cartilage defects observed upon knock down of miR-27. These data support a crucial role for miR-27 in promoting chondrogenic differentiation in the pharyngeal arches through regulation of FAK.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping