@article{85151,
  keywords = {Animals, Zebrafish, signal transduction, Mutation, Binding Sites, Protein Binding, Gene Expression, Xenopus Proteins, Xenopus laevis, Microtubules, Embryo, Nonmammalian, Zebrafish Proteins, Cell Movement, Skin, Kidney, Larva, Cell Polarity, Genetic Loci, CRISPR-Cas Systems, Cilia, Dishevelled Proteins, Homologous Recombination, LIM Domain Proteins},
  author = {Kimberly Jaffe and Daniel Grimes and Jodi Schottenfeld-Roames and Michael Werner and Tse-Shuen Ku and Sun Kim and Jose Pelliccia and Nicholas Morante and Brian Mitchell and Rebecca Burdine},
  title = {c21orf59/kurly Controls Both Cilia Motility and Polarization.},
  abstract = { Cilia are microtubule-based projections that function in the movement of extracellular fluid. This requires cilia to be: (1) motile and driven by dynein complexes and (2) correctly polarized on the surface of cells, which requires planar cell polarity (PCP). Few factors that regulate both processes have been discovered. We reveal that C21orf59/Kurly (Kur), a cytoplasmic protein with some enrichment at the base of cilia, is needed for motility; zebrafish mutants exhibit characteristic developmental abnormalities and dynein arm defects. kur was also required for proper cilia polarization in the zebrafish kidney and the larval skin of Xenopus laevis. CRISPR/Cas9 coupled with homologous recombination to disrupt the endogenous kur locus in Xenopus resulted in the asymmetric localization of the PCP protein Prickle2 being lost in mutant multiciliated cells. Kur also makes interactions with other PCP components, including Disheveled. This supports a model wherein Kur plays a dual role in cilia motility and polarization. },
  year = {2016},
  journal = {Cell Rep},
  volume = {14},
  pages = {1841-9},
  month = {03/2016},
  issn = {2211-1247},
  doi = {10.1016/j.celrep.2016.01.069},
  language = {eng},
}