Research ArticleDevelopmental Biology

Augmented BMP signaling commits cranial neural crest cells to a chondrogenic fate by suppressing autophagic β-catenin degradation

See allHide authors and affiliations

Science Signaling  12 Jan 2021:
Vol. 14, Issue 665, eaaz9368
DOI: 10.1126/scisignal.aaz9368

You are currently viewing the editor's summary.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

Altering cell fate through autophagy

Mutations that constitutively activate the bone morphogenetic protein (BMP) receptor ACVR1 lead to fibrodysplasia ossificans progressiva (FOP), a disease in which patients develop heterotopic bones through endochondral ossification in connective tissues. Yang et al. found that constitutively active ACVR1 caused cranial neural crest cells (CNCCs) in mice to adopt a chondrogenic fate, resulting in ectopic craniofacial cartilage. The increased BMP signaling caused this shift in cell fate by stimulating mTORC1 activity, which suppressed autophagic degradation of β-catenin and promoted chondrogenesis in CNCCs. These findings offer a possible explanation for the craniofacial cartilage abnormalities in FOP patients.

View Full Text

Stay Connected to Science Signaling