ArticleDevelopment (Cambridge, England)2011
BMP and non-canonical Wnt signaling are required for inhibition of secondary tail formation in zebrafish.
Article in Development (Cambridge, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Tbx16 and mesogenin 1 promote presomitic mesoderm differentiation by repressing the mesodermal progenitor cell state.PLoS genetics · 2026Article
- Unravelling the progression of the zebrafish primary body axis with reconstructed spatiotemporal transcriptomics.Genome biology · 2026Article
- Migration of Kupffer's vesicle-derived cells is essential for tail morphogenesis in zebrafish embryos.Development (Cambridge, England) · 2025Article
- Sizzled (Frzb3) physically interacts with noncanonical Wnt ligands to inhibit gastrulation cell movement.Molecules and cells · 2024Article
- Cercosporamide inhibits bone morphogenetic protein receptor type I kinase activity in zebrafish.Disease models & mechanisms · 2020Article
- Organization of Embryonic Morphogenesis via Mechanical Information.Developmental cell · 2019Article
- Mutational analysis of dishevelled genes in zebrafish reveals distinct functions in embryonic patterning and gastrulation cell movements.PLoS genetics · 2018Article
- The zebrafish tailbud contains two independent populations of midline progenitor cells that maintain long-term germ layer plasticity and differentiate in response to local signaling cues.Development (Cambridge, England) · 2016Article
- Article
- Amphioxus makes the cut-Again.Communicative & integrative biology · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The role of bone morphogenetic protein (BMP) signaling in specifying cell fate in the zebrafish tailbud has been well established. In addition to a loss of ventral tissues, such as ventral tailfin and cloaca, some embryos with compromised BMP signaling produce an additional phenotype: a ventrally located secondary tail containing both somitic muscle and notochord. This phenotype has been proposed to reflect a fate-patterning defect due to a change in a hypothesized BMP activity gradient. Here, we show that a defect in morphogenetic movements, not fate patterning, underlies the formation of secondary tails in BMP-inhibited embryos. Our data indicate that BMP signaling is activated in the ventroposterior tailbud to promote cell migration during tailbud protrusion, and that defective migration of these cells in BMP mutants ultimately leads to bifurcation of the caudal notochord. Additionally, we show that non-canonical Wnt signaling is also required for proper tail morphogenesis, possibly by maintaining cohesion of notochord progenitors by regulation of cadherin localization. We propose a model in which BMP and the non-canonical Wnt pathway regulate tail morphogenesis by controlling cell migration and cell adhesion within the tailbud.
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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.