PUBLICATION
Sox2 and Canonical Wnt Signaling Interact to Activate a Developmental Checkpoint Coordinating Morphogenesis with Mesoderm Fate Acquisition
- Authors
- Kinney, B.A., Al Anber, A., Row, R.H., Tseng, Y.J., Weidmann, M.D., Knaut, H., Martin, B.L.
- ID
- ZDB-PUB-201029-16
- Date
- 2020
- Source
- Cell Reports 33: 108311 (Journal)
- Registered Authors
- Knaut, Holger, Martin, Benjamin, Row, Richard H.
- Keywords
- canonical Wnt signaling, mesoderm, neuromesodermal progenitors, somite, sox2, spinal cord, tbx16, zebrafish
- MeSH Terms
-
- Animals
- Humans
- Mesoderm/metabolism*
- Morphogenesis
- SOXB1 Transcription Factors/metabolism*
- Wnt Signaling Pathway*
- PubMed
- 33113369 Full text @ Cell Rep.
Citation
Kinney, B.A., Al Anber, A., Row, R.H., Tseng, Y.J., Weidmann, M.D., Knaut, H., Martin, B.L. (2020) Sox2 and Canonical Wnt Signaling Interact to Activate a Developmental Checkpoint Coordinating Morphogenesis with Mesoderm Fate Acquisition. Cell Reports. 33:108311.
Abstract
Animal embryogenesis requires a precise coordination between morphogenesis and cell fate specification. During mesoderm induction, mesodermal fate acquisition is tightly coordinated with the morphogenetic process of epithelial-to-mesenchymal transition (EMT). In zebrafish, cells exist transiently in a partial EMT state during mesoderm induction. Here, we show that cells expressing the transcription factor Sox2 are held in the partial EMT state, stopping them from completing the EMT and joining the mesoderm. This is critical for preventing the formation of ectopic neural tissue. The mechanism involves synergy between Sox2 and the mesoderm-inducing canonical Wnt signaling pathway. When Wnt signaling is inhibited in Sox2-expressing cells trapped in the partial EMT, cells exit into the mesodermal territory but form an ectopic spinal cord instead of mesoderm. Our work identifies a critical developmental checkpoint that ensures that morphogenetic movements establishing the mesodermal germ layer are accompanied by robust mesodermal cell fate acquisition.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping