PUBLICATION

Core planar cell polarity genes VANGL1 and VANGL2 in predisposition to congenital vertebral malformations

Authors
Feng, X., Ye, Y., Zhang, J., Zhang, Y., Zhao, S., Mak, J.C.W., Otomo, N., Zhao, Z., Niu, Y., Yonezawa, Y., Li, G., Lin, M., Li, X., Cheung, P.W.H., Xu, K., Takeda, K., Wang, S., Xie, J., Kotani, T., Choi, V.N.T., Song, Y.Q., Yang, Y., Luk, K.D.K., Lee, K.S., Li, Z., Li, P.S., Leung, C.Y.H., Lin, X., Wang, X., Qiu, G., DISCO (Deciphering disorders Involving Scoliosis and COmorbidities) study group, Watanabe, K., Japanese Early Onset Scoliosis Research Group, Wu, Z., Posey, J.E., Ikegawa, S., Lupski, J.R., Cheung, J.P.Y., Zhang, T.J., Gao, B., Wu, N.
ID
ZDB-PUB-240427-8
Date
2024
Source
Proceedings of the National Academy of Sciences of the United States of America   121: e2310283121e2310283121 (Journal)
Registered Authors
Keywords
VANGL1/2, congenital scoliosis, congenital vertebral malformation, planar cell polarity (PCP), somite
MeSH Terms
  • Animals
  • Carrier Proteins*
  • Cell Polarity*/genetics
  • Female
  • Genetic Predisposition to Disease
  • Humans
  • Intracellular Signaling Peptides and Proteins/genetics
  • Intracellular Signaling Peptides and Proteins/metabolism
  • Membrane Proteins*/genetics
  • Membrane Proteins*/metabolism
  • Mice
  • Nerve Tissue Proteins/genetics
  • Nerve Tissue Proteins/metabolism
  • Scoliosis/congenital
  • Scoliosis/genetics
  • Scoliosis/metabolism
  • Spine*/abnormalities
  • Spine*/metabolism
  • Wnt Signaling Pathway/genetics
  • Zebrafish*/embryology
  • Zebrafish*/genetics
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed
38669183 Full text @ Proc. Natl. Acad. Sci. USA
Abstract
Congenital scoliosis (CS), affecting approximately 0.5 to 1 in 1,000 live births, is commonly caused by congenital vertebral malformations (CVMs) arising from aberrant somitogenesis or somite differentiation. While Wnt/ß-catenin signaling has been implicated in somite development, the function of Wnt/planar cell polarity (Wnt/PCP) signaling in this process remains unclear. Here, we investigated the role of Vangl1 and Vangl2 in vertebral development and found that their deletion causes vertebral anomalies resembling human CVMs. Analysis of exome sequencing data from multiethnic CS patients revealed a number of rare and deleterious variants in VANGL1 and VANGL2, many of which exhibited loss-of-function and dominant-negative effects. Zebrafish models confirmed the pathogenicity of these variants. Furthermore, we found that Vangl1 knock-in (p.R258H) mice exhibited vertebral malformations in a Vangl gene dose- and environment-dependent manner. Our findings highlight critical roles for PCP signaling in vertebral development and predisposition to CVMs in CS patients, providing insights into the molecular mechanisms underlying this disorder.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping