Craniofacial malformations are common structural birth defects and usually associate with abnormal development of pharyngeal arches. Although some microRNAs have been found to be implicated in chondrogenesis in vitro, few have been shown to be essential for cartilage and bone development at the whole organism level. In this study, we report that mir92a is highly enriched in the chondrogenic progenitors and that its inactivation results in loss of pharyngeal cartilage elements due to poor proliferation, impaired differentiation, and unsustainable survival of chondrogenic progenitors. The Bmp antagonist gene noggin3 (nog3) is a direct target of mir92a. Inactivation of mir92a stabilizes nog3 mRNA, leading to repression of Bmp signaling and abnormal behaviors of chondrogenic progenitors. In contrast, ectopic expression of mir92a duplex decreases nog3 mRNA levels and, as a result, derepresses Bmp signaling and promotes cell apoptosis. Therefore, mir92a acts to maintain Bmp activity during pharyngeal cartilage formation by targeting nog3.