ArticleDevelopmental biology2015
CRISPR/Cas9: An inexpensive, efficient loss of function tool to screen human disease genes in Xenopus.
Article in Developmental biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 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
89 citing papers in PubMed, 136 citations in OpenAlex.
- mRNA Microinjection for Gene Expression Studies in Xenopus laevis and Xenopus tropicalis.Methods in molecular biology (Clifton, N.J.) · 2026Article
- CRISPR-Mediated Gene Editing: Generating Gene Knockouts or Precision Base Changes in FMethods in molecular biology (Clifton, N.J.) · 2026Article
- TheBiomolecules · 2025Review
- Centriolar defects underlie a primary ciliary dyskinesia phenotype in an adenylate kinase 7 deficient ciliated epithelium.Developmental biology · 2025Article
- Phenotype to genotype: A new and rapid approach using whole-genome sequencing.PLoS genetics · 2025Article
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- The Heterotaxy Gene CCDC11 Is Important for Cytokinesis via RhoA Regulation.Cytoskeleton (Hoboken, N.J.) · 2025Article
- X-CRISP: Domain-Adaptable and Interpretable CRISPR Repair Outcome Prediction.bioRxiv : the preprint server for biology · 2025Article
- Autism gene variants disrupt enteric neuron migration and cause gastrointestinal dysmotility.Nature communications · 2025Article
- Genomic Complexity ofmicroPublication biology · 2025Article
- Xenopus as a model system for studying pigmentation and pigmentary disorders.Pigment cell & melanoma research · 2025Review
- X-CRISP: domain-adaptable and interpretable CRISPR repair outcome prediction.Bioinformatics advances · 2025Article
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- CC2D1A causes ciliopathy, intellectual disability, heterotaxy, renal dysplasia, and abnormal CSF flow.Life science alliance · 2024Article
- AP2A2 mutation and defective endocytosis in a Malian family with hereditary spastic paraplegia.Neurobiology of disease · 2024Article
- Modelling human genetic disorders in Xenopus tropicalis.Disease models & mechanisms · 2024Review
- Diphthamide deficiency promotes association of eEF2 with p53 to induce p21 expression and neural crest defects.Nature communications · 2024Article
- A novel SMARCC1 BAFopathy implicates neural progenitor epigenetic dysregulation in human hydrocephalus.Brain : a journal of neurology · 2024Article
- Mitochondrial leak metabolism induces the Spemann-Mangold Organizer via Hif-1α in Xenopus.Developmental cell · 2023Article
- Expanding EMC foldopathies: Topogenesis deficits alter the neural crest.Genesis (New York, N.Y. : 2000) · 2023Article
29 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Congenital malformations are the major cause of infant mortality in the US and Europe. Due to rapid advances in human genomics, we can now efficiently identify sequence variants that may cause disease in these patients. However, establishing disease causality remains a challenge. Additionally, in the case of congenital heart disease, many of the identified candidate genes are either novel to embryonic development or have no known function. Therefore, there is a pressing need to develop inexpensive and efficient technologies to screen these candidate genes for disease phenocopy in model systems and to perform functional studies to uncover their role in development. For this purpose, we sought to test F0 CRISPR based gene editing as a loss of function strategy for disease phenocopy in the frog model organism, Xenopus tropicalis. We demonstrate that the CRISPR/Cas9 system can efficiently modify both alleles in the F0 generation within a few hours post fertilization, recapitulating even early disease phenotypes that are highly similar to knockdowns from morpholino oligos (MOs) in nearly all cases tested. We find that injecting Cas9 protein is dramatically more efficacious and less toxic than cas9 mRNA. We conclude that CRISPR based F0 gene modification in X. tropicalis is efficient and cost effective and readily recapitulates disease and MO phenotypes.
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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.