ArticleInvestigative ophthalmology & visual science2016
Loss of Axin2 Causes Ocular Defects During Mouse Eye Development.
Article in Investigative ophthalmology & visual science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Two novel AXIN2 variants in isolated tooth agenesis and the AXIN2-associated tooth agenesis pattern.BMC oral health · 2025Pooled it
- Novel mutations of AXIN2 identified in a Chinese Congenital Heart Disease Cohort.Journal of human genetics · 2019Trial
- DKK1 Targeting in Corneal Schwann Cells Rescues Axonal Regeneration and Mechanosensory Function After Corneal Injury.Journal of neuroscience research · 2026Article
- Direct Comparison of Constitutive Rax-Cre Transgenic Drivers That Activate in the Mouse Embryonic Eye Field.Investigative ophthalmology & visual science · 2026Article
- Axin1 stabilizes S-opsin and maintains cone photoreceptor survival by inhibiting GSK3β activity.Cell death discovery · 2026Article
- Direct comparison of constitutive Rax-Cre transgenic drivers that activate in the mouse embryonic eye field.bioRxiv : the preprint server for biology · 2025Article
- Loss of Cdc42 causes abnormal optic cup morphogenesis and microphthalmia in mouse.bioRxiv : the preprint server for biology · 2024Article
- The development and the genetic diseases of the ciliary body.Cell insight · 2024Review
- Loss of Cdc42 causes abnormal optic cup morphogenesis and microphthalmia in mouse.Frontiers in cellular neuroscience · 2024Article
- Wnt/β-catenin signaling controls mouse eyelid growth by mediating epithelial-mesenchymal interactions.The ocular surface · 2023Article
- Genome-wide screening reveals the genetic basis of mammalian embryonic eye development.BMC biology · 2023Article
- Article
- Porcn is essential for growth and invagination of the mammalian optic cup.Frontiers in cell and developmental biology · 2022Article
- Nf2 fine-tunes proliferation and tissue alignment during closure of the optic fissure in the embryonic mouse eye.Human molecular genetics · 2020Article
- The transcription factorDisease models & mechanisms · 2020Article
- De Novo Missense Variants in FBXW11 Cause Diverse Developmental Phenotypes Including Brain, Eye, and Digit Anomalies.American journal of human genetics · 2019Article
- An update on the genetics of ocular coloboma.Human genetics · 2019Review
- Conversations with Ray Guillery on albinism: linking Siamese cat visual pathway connectivity to mouse retinal development.The European journal of neuroscience · 2019Review
- Retinal Ganglion Cell Replacement: Current Status and Challenges Ahead.Developmental dynamics : an official publication of the American Association of Anatomists · 2019Review
- Spatiotemporal dynamics of canonical Wnt signaling during embryonic eye development and posterior capsular opacification (PCO).Experimental eye research · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
purposeThe scaffold protein Axin2 is an antagonist and universal target of the Wnt/β-catenin pathway. Disruption of Axin2 may lead to developmental eye defects; however, this has not been examined. The purpose of this study was to investigate the role of Axin2 during ocular and extraocular development in mouse.
methodsAnimals heterozygous and homozygous for a Axin2lacZ knock-in allele were analyzed at different developmental stages for reporter expression, morphology as well as for the presence of ocular and extraocular markers using histologic and immunohistochemical techniques.
resultsDuring early eye development, the Axin2lacZ reporter was expressed in the periocular mesenchyme, RPE, and optic stalk. In the developing retina, Axin2lacZ reporter expression was initiated in ganglion cells at late embryonic stages and robustly expressed in subpopulations of amacrine and horizontal cells postnatally. Activation of the Axin2lacZ reporter overlapped with labeling of POU4F1, PAX6, and Calbindin. Germline deletion of Axin2 led to variable ocular phenotypes ranging from normal to severely defective eyes exhibiting microphthalmia, coloboma, lens defects, and expanded ciliary margin. These defects were correlated with abnormal tissue patterning in individual affected tissues, such as the optic fissure margins in the ventral optic cup and in the expanded ciliary margin.
conclusionsOur results reveal a critical role for Axin2 during ocular development, likely by restricting the activity of the Wnt/β-catenin pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.