ArticlePloS one2014
Loss of FTO antagonises Wnt signaling and leads to developmental defects associated with ciliopathies.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- mRNA (New York, N.Y.) · 2025Article
- White Adipocyte Stem Cell Expansion Through Infant Formula Feeding: New Insights into Epigenetic Programming Explaining the Early Protein Hypothesis of Obesity.International journal of molecular sciences · 2025Review
- Technologies, strategies, and cautions when deconvoluting genome-wide association signals: FTO in focus.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2023Review
- The m6A(m)-independent role of FTO in regulating WNT signaling pathways.Life science alliance · 2022Article
- Article
- Single-Cell RNA Sequencing Characterizes the Molecular Heterogeneity of the Larval Zebrafish Optic Tectum.Frontiers in molecular neuroscience · 2022Article
- Role of N6-methyl-adenosine modification in mammalian embryonic development.Genetics and molecular biology · 2021Article
- m6A RNA Methylation: Ramifications for Gene Expression and Human Health.Molecular biotechnology · 2020Review
- A genetic signature of the evolution of loss of flight in the Galapagos cormorant.Science (New York, N.Y.) · 2017Article
- Utilizing the chicken as an animal model for human craniofacial ciliopathies.Developmental biology · 2016Review
- Hypomorphism of Fto and Rpgrip1l causes obesity in mice.The Journal of clinical investigation · 2016Article
- A patient with a novel homozygous missense mutation in FTO and concomitant nonsense mutation in CETP.Journal of human genetics · 2016Article
- FTO modulates fibrogenic responses in obstructive nephropathy.Scientific reports · 2016Article
- Zebrafish: a vertebrate tool for studying basal body biogenesis, structure, and function.Cilia · 2016Review
- Recent Progress in the Understanding of Obesity: Contributions of Genome-Wide Association Studies.Current obesity reports · 2015Review
- Using the avian mutant talpid2 as a disease model for understanding the oral-facial phenotypes of oral-facial-digital syndrome.Disease models & mechanisms · 2015Article
- Evaluation of zebrafish kidney function using a fluorescent clearance assay.Journal of visualized experiments : JoVE · 2015Article
- The ciliary baton: orchestrating neural crest cell development.Current topics in developmental biology · 2015Review
- Hypomorphism for RPGRIP1L, a ciliary gene vicinal to the FTO locus, causes increased adiposity in mice.Cell metabolism · 2014Article
- Modify or die?--RNA modification defects in metazoans.RNA biology · 2014Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Common intronic variants in the Human fat mass and obesity-associated gene (FTO) are found to be associated with an increased risk of obesity. Overexpression of FTO correlates with increased food intake and obesity, whilst loss-of-function results in lethality and severe developmental defects. Despite intense scientific discussions around the role of FTO in energy metabolism, the function of FTO during development remains undefined. Here, we show that loss of Fto leads to developmental defects such as growth retardation, craniofacial dysmorphism and aberrant neural crest cells migration in Zebrafish. We find that the important developmental pathway, Wnt, is compromised in the absence of FTO, both in vivo (zebrafish) and in vitro (Fto(-/-) MEFs and HEK293T). Canonical Wnt signalling is down regulated by abrogated β-Catenin translocation to the nucleus whilst non-canonical Wnt/Ca(2+) pathway is activated via its key signal mediators CaMKII and PKCδ. Moreover, we demonstrate that loss of Fto results in short, absent or disorganised cilia leading to situs inversus, renal cystogenesis, neural crest cell defects and microcephaly in Zebrafish. Congruently, Fto knockout mice display aberrant tissue specific cilia. These data identify FTO as a protein-regulator of the balanced activation between canonical and non-canonical branches of the Wnt pathway. Furthermore, we present the first evidence that FTO plays a role in development and cilia formation/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.