PUBLICATION
The signalling receptor MCAM coordinates apical-basal polarity and planar cell polarity during morphogenesis
- Authors
- Gao, Q., Zhang, J., Wang, X., Liu, Y., He, R., Liu, X., Wang, F., Feng, J., Yang, D., Wang, Z., Meng, A., Yan, X.
- ID
- ZDB-PUB-170608-5
- Date
- 2017
- Source
- Nature communications 8: 15279 (Journal)
- Registered Authors
- Liu, Ying, Meng, Anming, Zhang, Junfeng
- Keywords
- Body patterning, Cell polarity
- MeSH Terms
-
- HEK293 Cells
- Xenopus Proteins/metabolism*
- Protein Transport
- Body Patterning
- CD146 Antigen/metabolism*
- PubMed
- 28589943 Full text @ Nat. Commun.
Abstract
The apical-basal (AB) polarity and planar cell polarity (PCP) provide an animal cell population with different phenotypes during morphogenesis. However, how cells couple these two patterning systems remains unclear. Here we provide in vivo evidence that melanoma cell adhesion molecule (MCAM) coordinates AB polarity-driven lumenogenesis and c-Jun N-terminal kinase (JNK)/PCP-dependent ciliogenesis. We identify that MCAM is an independent receptor of fibroblast growth factor 4 (FGF4), a membrane anchor of phospholipase C-γ (PLC-γ), an immediate upstream receptor of nuclear factor of activated T-cells (NFAT) and a constitutive activator of JNK. We find that MCAM-mediated vesicular trafficking towards FGF4, while generating a priority-grade transcriptional response of NFAT determines lumenogenesis. We demonstrate that MCAM plays indispensable roles in ciliogenesis through activating JNK independently of FGF signals. Furthermore, mcam-deficient zebrafish and Xenopus exhibit a global defect in left-right (LR) asymmetric establishment as a result of morphogenetic failure of their LR organizers. Therefore, MCAM coordination of AB polarity and PCP provides insight into the general mechanisms of morphogenesis.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping