PUBLICATION

Zebrafish Prickle1b mediates facial branchiomotor neuron migration via a farnesylation-dependent nuclear activity

Authors
Mapp, O.M., Walsh, G.S., Moens, C.B., Tada, M., and Prince, V.E.
ID
ZDB-PUB-110518-43
Date
2011
Source
Development (Cambridge, England)   138(10): 2121-2132 (Journal)
Registered Authors
Mapp, Oni, Moens, Cecilia, Prince, Victoria E., Tada, Masazumi, Walsh, Gregory
Keywords
facial branchiomotor neurons, Prickle1b, neuronal migration, REST, farnesylation, zebrafish
MeSH Terms
  • Models, Biological
  • Gene Knockdown Techniques
  • Adaptor Proteins, Signal Transducing
  • Cell Movement
  • Gene Expression Regulation, Developmental
  • Mutation
  • Sequence Homology, Amino Acid
  • Molecular Sequence Data
  • Base Sequence
  • Cell Nucleus/metabolism
  • Protein Prenylation
  • Hydroxymethylglutaryl CoA Reductases/metabolism
  • Amino Acid Sequence
  • Zebrafish Proteins/antagonists & inhibitors
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
  • Neurogenesis
  • Animals, Genetically Modified
  • Farnesyltranstransferase/metabolism
  • Motor Neurons/cytology
  • Motor Neurons/metabolism
  • Animals
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish/metabolism*
  • DNA, Complementary/genetics
  • Repressor Proteins/genetics
  • Repressor Proteins/metabolism
  • Carrier Proteins/antagonists & inhibitors
  • Carrier Proteins/genetics
  • Carrier Proteins/metabolism*
  • Signal Transduction
  • LIM Domain Proteins
(all 33)
PubMed
21521740 Full text @ Development
Abstract
The facial branchiomotor neurons (FBMNs) undergo a characteristic tangential migration in the vertebrate hindbrain. We previously used a morpholino knockdown approach to reveal that zebrafish prickle1b (pk1b) is required for this migration. Here we report that FBMN migration is also blocked in a pk1b mutant with a disruption in the consensus farnesylation motif. We confirmed that this lipid modification is required during FBMN migration by disrupting the function of farnesyl biosynthetic enzymes. Furthermore, farnesylation of a tagged Pk1b is required for its nuclear localization. Using a unique rescue approach, we have demonstrated that Pk1b nuclear localization and farnesylation are required during FBMN migration. Our data suggest that Pk1b acts at least partially independently of core planar cell polarity molecules at the plasma membrane, and might instead be acting at the nucleus. We also found that the neuronal transcriptional silencer REST is necessary for FBMN migration, and we provide evidence that interaction between Pk1b and REST is required during this process. Finally, we demonstrate that REST protein, which is normally localized in the nuclei of migrating FBMNs, is depleted from the nuclei of Pk1b-deficient neurons. We conclude that farnesylation-dependent nuclear localization of Pk1b is required to regulate REST localization and thus FBMN migration.
Genes / Markers
Figures
Figure Gallery (10 images)
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Expression
Phenotype
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
ch100TgTransgenic Insertion
    fh122
      Point Mutation
      rw0TgTransgenic Insertion
        s617
          Point Mutation
          1 - 4 of 4
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          Human Disease / Model
          No data available
          Sequence Targeting Reagents
          Target Reagent Reagent Type
          fntbMO1-fntbMRPHLNO
          hmgcrbMO1-hmgcrbMRPHLNO
          pggt1bMO2-pggt1bMRPHLNO
          prickle1bMO1-prickle1bMRPHLNO
          prickle1bMO2-prickle1bMRPHLNO
          restMO1-restMRPHLNO
          1 - 6 of 6
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          Fish
          Antibodies
          Name Type Antigen Genes Isotypes Host Organism
          Ab1-restpolyclonalRabbit
          1 - 1 of 1
          Show
          Orthology
          No data available
          Engineered Foreign Genes
          Marker Marker Type Name
          GFPEFGGFP
          mRFPEFGmRFP
          1 - 2 of 2
          Show
          Mapping
          No data available