Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Non-Canonical Wnt Signaling Pathways

Non-Canonical Wnt Signaling Pathways

Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...

Non-Canonical Wnt Signaling Pathways

Non-Canonical Wnt Signaling Pathways

Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...

Canonical Wnt Signaling Pathway

Canonical Wnt Signaling Pathway

The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which results in tumor...

Canonical Wnt Signaling Pathway

Canonical Wnt Signaling Pathway

The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which results in tumor...

Pleiotropy

Pleiotropy

Pleiotropy is the phenomenon in which a single gene impacts multiple, seemingly unrelated phenotypic traits. For example, defects in the SOX10 gene cause Waardenburg Syndrome Type 4, or WS4, which can cause defects in pigmentation, hearing impairments, and an absence of intestinal contractions necessary for elimination. This diversity of phenotypes results from the expression pattern of SOX10 in early embryonic and fetal development. SOX10 is found in neural crest cells that form melanocytes,...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

A Wnt-induced conformational phospho-switch in DVL3 controls association with Frizzled receptors and Wnt/β-catenin signaling.

Science advances·2026

Same author

Modeling Disease-Relevant Bile Duct Morphogenesis Defects in a Tunable In Vitro System.

ACS biomaterials science & engineering·2026

Same author

Improved functional JAG1 and NOTCH2 variant testing in patients with clinical or suspected Alagille syndrome using new low-Notch activity cells.

Human genetics·2026

Same author

Single-cell, clonal and spatial atlases of cranial placodes illuminate their specification and evolution.

bioRxiv : the preprint server for biology·2026

Same author

Casein kinase 1δ/ε inhibition suppresses CLL proliferation through cell-intrinsic and microenvironmental mechanisms.

HemaSphere·2026

Same author

Distinct radial glia subtypes regulate midbrain dopaminergic neuron development.

Nature neuroscience·2026

Search research articles

Related Experiment Video

Updated: Jun 19, 2026

Modeling Paracrine Noncanonical Wnt Signaling In Vitro

Modeling Paracrine Noncanonical Wnt Signaling In Vitro

Published on: December 10, 2021

Genetic interaction between Lrp6 and Wnt5a during mouse development.

Emma R Andersson¹, Lenka Bryjova, Kristin Biris

¹Molecular Neurobiology, Department of Medical Biochemistry & Biophysics, Karolinska Institutet, Stockholm, Sweden.

Developmental Dynamics : an Official Publication of the American Association of Anatomists

|October 2, 2009

Summary

This summary is machine-generated.

Loss of Lrp6 worsens Wnt5a signaling defects in mice, causing severe developmental issues like spina bifida and neurogenesis failure. These findings highlight the complex interplay between Wnt5a and Lrp6 during embryonic development.

More Related Videos

The Power of Simplicity: Sea Urchin Embryos as in Vivo Developmental Models for Studying Complex Cell-to-cell Signaling Network Interactions

The Power of Simplicity: Sea Urchin Embryos as in Vivo Developmental Models for Studying Complex Cell-to-cell Signaling Network Interactions

Published on: February 16, 2017

Related Experiment Videos

Last Updated: Jun 19, 2026

Modeling Paracrine Noncanonical Wnt Signaling In Vitro

Modeling Paracrine Noncanonical Wnt Signaling In Vitro

Published on: December 10, 2021

The Power of Simplicity: Sea Urchin Embryos as in Vivo Developmental Models for Studying Complex Cell-to-cell Signaling Network Interactions

The Power of Simplicity: Sea Urchin Embryos as in Vivo Developmental Models for Studying Complex Cell-to-cell Signaling Network Interactions

Published on: February 16, 2017

Area of Science:

Developmental Biology
Molecular Biology
Genetics

Background:

Lrp6 acts as a receptor in Wnt/beta-catenin signaling.
Wnt5a typically activates noncanonical Wnt signaling, not Wnt/beta-catenin.
Previous work showed Lrp6 inhibits Wnt5a/Wnt11 signaling.

Purpose of the Study:

To investigate the combined effects of Wnt5a and Lrp6 loss-of-function in mouse development.
To further elucidate the complex interactions between Wnt5a and Lrp6 signaling pathways.

Main Methods:

Analysis of compound Wnt5a/Lrp6 mutant mice.
Phenotypic characterization of embryos with combined Wnt5a and Lrp6 loss-of-function.

Main Results:

Lrp6 haploinsufficiency in Wnt5a-/- mice caused spina bifida and posterior truncation.
Wnt5a-/-Lrp6-/- embryos exhibited severe defects in mesoderm morphogenesis, somitogenesis, and neurogenesis.
Compound mutants displayed exacerbated phenotypes compared to single mutants.

Conclusions:

Wnt5a and Lrp6 have complex, often opposing, roles during mouse development.
Cooperation and antagonism between Wnt5a and Lrp6 are critical for normal embryonic morphogenesis.
These findings add complexity to the understanding of Wnt signaling in development.