ArticlePloS one2013
Identification of an evx1-dependent joint-formation pathway during FIN regeneration.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Overexpression of potassium channel Kcna5 alters skeletal patterning in the zebrafish regenerating fin.Developmental biology · 2025Article
- Compartmentalization and synergy of osteoblasts drive bone formation in the regenerating fin.iScience · 2024Article
- Retinoic Acid InfluencesBioelectricity · 2023Article
- Gene expression patterns associated with caudal fin shape in the cichlidHydrobiologia · 2023Article
- longfin causes cis-ectopic expression of the kcnh2a ether-a-go-go K+ channel to autonomously prolong fin outgrowth.Development (Cambridge, England) · 2021Article
- Article
- Connexin 43 gap junctional intercellular communication inhibitsDevelopment (Cambridge, England) · 2020Article
- Gene expression profiling suggests differences in molecular mechanisms of fin elongation between cichlid species.Scientific reports · 2019Article
- Collagen COL22A1 maintains vascular stability and mutations inDisease models & mechanisms · 2018Article
- Simplet-dependent regulation of β-catenin signaling influences skeletal patterning downstream of Cx43.Development (Cambridge, England) · 2018Article
- Towards a gene regulatory network shaping the fins of the Princess cichlid.Scientific reports · 2018Article
- Connexin Communication Compartments and Wound Repair in Epithelial Tissue.International journal of molecular sciences · 2018Review
- Bioelectric signaling in regeneration: Mechanisms of ionic controls of growth and form.Developmental biology · 2018Review
- Cohesin mediates Esco2-dependent transcriptional regulation in a zebrafish regenerating fin model of Roberts Syndrome.Biology open · 2017Article
- A gene expression study of ornamental fin shape in Neolamprologus brichardi, an African cichlid species.Scientific reports · 2017Article
- Cx43 suppresses evx1 expression to regulate joint initiation in the regenerating fin.Developmental dynamics : an official publication of the American Association of Anatomists · 2017Article
- Gap junctional signaling in pattern regulation: Physiological network connectivity instructs growth and form.Developmental neurobiology · 2017Review
- Building and maintaining joints by exquisite local control of cell fate.Wiley interdisciplinary reviews. Developmental biology · 2017Review
- Cx43-Dependent Skeletal Phenotypes Are Mediated by Interactions between the Hapln1a-ECM and Sema3d during Fin Regeneration.PloS one · 2016Article
- Re-membering the body: applications of computational neuroscience to the top-down control of regeneration of limbs and other complex organs.Integrative biology : quantitative biosciences from nano to macro · 2015Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Joints are essential for skeletal flexibly and form, yet the process underlying joint morphogenesis is poorly understood. Zebrafish caudal fins are comprised of numerous segmented bony fin rays, where growth occurs by the sequential addition of new segments and new joints. Here, we evaluate joint gene expression during fin regeneration. First, we identify three genes that influence joint formation, evx1, dlx5a, and mmp9. We place these genes in a common molecular pathway by evaluating both their expression patterns along the distal-proximal axis (i.e. where the youngest tissue is always the most distal), and by evaluating changes in gene expression following gene knockdown. Prior studies from our lab indicate that the gap junction protein Cx43 suppresses joint formation. Remarkably, changes in Cx43 activity alter the expression of joint markers. For example, the reduced levels of Cx43 in the sof (b123) mutant causes short fin ray segments/premature joints. We also find that the expression of evx1-dlx5a-mmp9 is shifted distally in sof (b123) , consistent with premature expression of these genes. In contrast, increased Cx43 in the alf (dty86) mutant leads to stochastic joint failure and stochastic loss of evx1 expression. Indeed, reducing the level of Cx43 in alf (dty86) rescues both the evx1 expression and joint formation. These results suggest that Cx43 influences the pattern of joint formation by influencing the timing of evx1 expression.
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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.