ArticleDisease models & mechanisms2022
The role of Lrp6-mediated Wnt/β-catenin signaling in the development and intervention of spinal neural tube defects in mice.
Article in Disease models & mechanisms, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Dual repression modes triggered by constitutively stabilized beta-catenin in the dorsal neural tube underlie cell fate alterations of the roof plate, neural crest, and dorsal interneurons.Cell & bioscience · 2026Article
- The significance of calcium ions in cerebral ischemia-reperfusion injury: mechanisms and intervention strategies.Frontiers in molecular biosciences · 2025Review
- National strategies for screening neural tube defects in Saudi Arabia: activating prevention and early intervention.Frontiers in public health · 2025Review
- Parental arsenic exposure and tissue-specific DNA methylation in Bangladeshi infants with spina bifida.Epigenetics · 2024Article
- Epigenetic regulation by TET1 in gene-environmental interactions influencing susceptibility to congenital malformations.bioRxiv : the preprint server for biology · 2024Article
- A rationally designed optochemogenetic switch for activating canonical Wnt signaling.iScience · 2023Article
- Balancing WNT signalling in early forebrain development: The role of LRP4 as a modulator of LRP6 function.Frontiers in cell and developmental biology · 2023Article
- Wnt/planar cell polarity signaling controls morphogenetic movements of gastrulation and neural tube closure.Cellular and molecular life sciences : CMLS · 2022Review
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Authors and funding
6 authors at 1 institution in 1 country.
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Abstract
Neural tube defects (NTDs) are among the common and severe birth defects with poorly understood etiology. Mutations in the Wnt co-receptor LRP6 are associated with NTDs in humans. Either gain-of-function (GOF) or loss-of-function (LOF) mutations of Lrp6 can cause NTDs in mice. NTDs in Lrp6-GOF mutants may be attributed to altered β-catenin-independent noncanonical Wnt signaling. However, the mechanisms underlying NTDs in Lrp6-LOF mutants and the role of Lrp6-mediated canonical Wnt/β-catenin signaling in neural tube closure remain unresolved. We previously demonstrated that β-catenin signaling is required for posterior neuropore (PNP) closure. In the current study, conditional ablation of Lrp6 in dorsal PNP caused spinal NTDs with diminished activities of Wnt/β-catenin signaling and its downstream target gene Pax3, which is required for PNP closure. β-catenin-GOF rescued NTDs in Lrp6-LOF mutants. Moreover, maternal supplementation of a Wnt/β-catenin signaling agonist reduced the frequency and severity of spinal NTDs in Lrp6-LOF mutants by restoring Pax3 expression. Together, these results demonstrate the essential role of Lrp6-mediated Wnt/β-catenin signaling in PNP closure, which could also provide a therapeutic target for NTD intervention through manipulation of canonical Wnt/β-catenin signaling activities.
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