ArticlePLoS genetics2012
The tumor suppressor gene retinoblastoma-1 is required for retinotectal development and visual function in zebrafish.
Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 35 citations in OpenAlex.
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- cacna2d3, a voltage-gated calcium channel subunit, functions in vertebrate habituation learning and the startle sensitivity threshold.PloS one · 2022Article
- Xanthatin Selectively Targets Retinoblastoma by Inhibiting the PLK1-Mediated Cell Cycle.Investigative ophthalmology & visual science · 2021Article
- Pregnancy-associated plasma protein-aa regulates endoplasmic reticulum-mitochondria associations.eLife · 2021Article
- Pregnancy-associated plasma protein-aa supports hair cell survival by regulating mitochondrial function.eLife · 2019Article
- The ubiquitin ligase PHR promotes directional regrowth of spinal zebrafish axons.Communications biology · 2019Article
- Epigenetic regulators Rbbp4 and Hdac1 are overexpressed in a zebrafish model of RB1 embryonal brain tumor, and are required for neural progenitor survival and proliferation.Disease models & mechanisms · 2018Article
- Heterogeneity in retinoblastoma: a tale of molecules and models.Clinical and translational medicine · 2017Review
- Zebrafish sin3b mutants are viable but have size, skeletal, and locomotor defects.Developmental dynamics : an official publication of the American Association of Anatomists · 2017Article
- Coordinating progenitor cell cycle exit and differentiation in the developing vertebrate retina.Neurogenesis (Austin, Tex.) · 2016Article
- Cell cycle control in the early embryonic development of aquatic animal species.Comparative biochemistry and physiology. Toxicology & pharmacology : CBP · 2015Review
- The LRR receptor Islr2 is required for retinal axon routing at the vertebrate optic chiasm.Neural development · 2015Article
- Rapid tumor induction in zebrafish by TALEN-mediated somatic inactivation of the retinoblastoma1 tumor suppressor rb1.Scientific reports · 2015Article
- Cross-tissue and cross-species analysis of gene expression in skeletal muscle and electric organ of African weakly-electric fish (Teleostei; Mormyridae).BMC genomics · 2015Article
- A convergent and essential interneuron pathway for Mauthner-cell-mediated escapes.Current biology : CB · 2015Article
- A genome-wide screen identifies PAPP-AA-mediated IGFR signaling as a novel regulator of habituation learning.Neuron · 2015Article
- Zebrafish foxc1a drives appendage-specific neural circuit development.Development (Cambridge, England) · 2015Article
- Sensory hair cell regeneration in the zebrafish lateral line.Developmental dynamics : an official publication of the American Association of Anatomists · 2014Review
- Distinct tissue-specific requirements for the zebrafish tbx5 genes during heart, retina and pectoral fin development.Open biology · 2014Article
- Mirror movement-like defects in startle behavior of zebrafish dcc mutants are caused by aberrant midline guidance of identified descending hindbrain neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in the retinoblastoma tumor suppressor gene (rb1) cause both sporadic and familial forms of childhood retinoblastoma. Despite its clinical relevance, the roles of rb1 during normal retinotectal development and function are not well understood. We have identified mutations in the zebrafish space cadet locus that lead to a premature truncation of the rb1 gene, identical to known mutations in sporadic and familial forms of retinoblastoma. In wild-type embryos, axons of early born retinal ganglion cells (RGC) pioneer the retinotectal tract to guide later born RGC axons. In rb1 deficient embryos, these early born RGCs show a delay in cell cycle exit, causing a transient deficit of differentiated RGCs. As a result, later born mutant RGC axons initially fail to exit the retina, resulting in optic nerve hypoplasia. A significant fraction of mutant RGC axons eventually exit the retina, but then frequently project to the incorrect optic tectum. Although rb1 mutants eventually establish basic retinotectal connectivity, behavioral analysis reveals that mutants exhibit deficits in distinct, visually guided behaviors. Thus, our analysis of zebrafish rb1 mutants reveals a previously unknown yet critical role for rb1 during retinotectal tract development and visual function.
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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.