Wnt-Dependent Activation of ERK Mediates Repression of Chondrocyte Fate during Calvarial Development
Year: 2021
Type: article
Abstract: Wnt signaling regulates cell fate decisions in diverse contexts during development, and loss of Wnt signaling in the cranial mesenchyme results in a robust and binary cell fate switch from cranial bone to ectopic cartilage. The Extracellular signal-regulated protein kinase 1 and 2 (ERK1/2) and Wnt signaling pathways are activated during calvarial osteoblast cell fate selection. Here, we test the hypothesis that ERK signaling is a mediator of Wnt-dependent cell fate decisions in the cranial mesenchyme. First, we show that loss of Erk1/ 2 in the cranial mesenchyme results in a diminished domain of osteoblast marker expression and increased expression of cartilage fate markers and ectopic cartilage formation in the frontal bone primordia. Second, we show that mesenchyme Wnt/β-catenin signaling and Wntless are required for ERK activation in calvarial osteoblasts. Third, we demonstrate that Wnt and ERK signaling pathways function together to repress Sox9 expression in mouse cranial mesenchyme. Our results demonstrate a link between the Wnt and ERK signaling pathways in regulating lineage selection in a subset of calvarial cells and provide new insights into Wnt-dependent cell fate decisions.
Source: Journal of Developmental Biology
DOI: 10.3390/jdb9030023
Authors: Beatriz Ibarra, Cody Machen, Radhika P. Atit
Institution: Case Western Reserve University
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $1,728
Awards: G1890173913, G3549828030, G3679713553, Training Program in Musculoskeletal Research, G5528342922, G7023953676, Acquisition of a Leica TCS SP5 Confocal Microscope For A Multi-User Facility, Genetic mechanisms of craniofacial dermal development, G8548820625, Phospho-ERK1/2 in beta-catenin-dependent cranial lineage restriction, Mechanisms of apical expansion in calvarial bone morphogenesis
OpenAlex ID: W3157464678
