ArticleScientific reports2016
The nephronophthisis-related gene ift-139 is required for ciliogenesis in Caenorhabditis elegans.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
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- Integrative modeling reveals the molecular architecture of the intraflagellar transport A (IFT-A) complex.eLife · 2022Article
- On the Wrong Track: Alterations of Ciliary Transport in Inherited Retinal Dystrophies.Frontiers in cell and developmental biology · 2021Review
- Disease Modeling To Understand the Pathomechanisms of Human Genetic Kidney Disorders.Clinical journal of the American Society of Nephrology : CJASN · 2020Review
- Ttc21b Is Required in Bergmann Glia for Proper Granule Cell Radial Migration.Journal of developmental biology · 2017Article
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- Immobilization of Caenorhabditis elegans to Analyze Intracellular Transport in Neurons.Journal of visualized experiments : JoVE · 2017Article
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Abstract
Defects in cilia cause a spectrum of diseases known as ciliopathies. Nephronophthisis, a ciliopathy, is the most common genetic cause of renal disease. Here, I cloned and analysed a nephronophthisis-related gene ift-139 in Caenorhabditis elegans. ift-139 was exclusively expressed in ciliated neurons in C. elegans. Genetic and cellular analyses suggest that ift-139 plays a role in retrograde intraflagellar transport and is required for cilia formation. A homologous point mutation that causes ciliopathy disrupted the function of ift-139 in C. elegans. ift-139 is an orthologue of human TTC21B, mutations in which are known to cause nephronophthisis 12 and short-rib thoracic dysplasia 4. These results suggest that ift-139 is evolutionarily conserved and fundamental to the formation of cilia.
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