miR-27 regulates chondrogenesis by suppressing focal adhesion kinase during pharyngeal arch development.

Kara N, Wei C, Commanday AC, Patton JG
Dev Biol. 2017 429 (1): 321-334

PMID: 28625871 · PMCID: PMC5582384 · DOI:10.1016/j.ydbio.2017.06.013

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.

Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.

MeSH Terms (16)

Animal Fins Animals Branchial Region Cartilage Cell Differentiation Cell Proliferation Cell Survival Chondrogenesis Embryo, Nonmammalian Focal Adhesion Protein-Tyrosine Kinases Gene Expression Regulation, Developmental Gene Knockdown Techniques MicroRNAs Morphogenesis Neural Crest Zebrafish

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