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
-
- Branchial Region/embryology*
- Branchial Region/enzymology*
- Cell Differentiation/genetics
- Morphogenesis/genetics
- Neural Crest/cytology
- PubMed
- 28625871 Full text @ Dev. Biol.
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.
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