PUBLICATION

Different roles for KIF17 and kinesin II in photoreceptor development and maintenance

Authors
Insinna, C., Humby, M., Sedmak, T., Wolfrum, U., and Besharse, J.C.
ID
ZDB-PUB-090424-25
Date
2009
Source
Developmental Dynamics : an official publication of the American Association of Anatomists   238(9): 2211-2222 (Journal)
Registered Authors
Keywords
KIF17, kinesin II, photoreceptors, ciliogenesis, IFT
MeSH Terms
  • Animals
  • Blotting, Western
  • Embryo, Nonmammalian/drug effects
  • Embryo, Nonmammalian/metabolism
  • Embryo, Nonmammalian/ultrastructure
  • Immunohistochemistry
  • Immunoprecipitation
  • Kinesins/genetics
  • Kinesins/metabolism
  • Kinesins/pharmacology
  • Kinesins/physiology*
  • Mice
  • Microscopy, Electron, Transmission
  • Microscopy, Immunoelectron
  • Retinal Cone Photoreceptor Cells/metabolism*
  • Retinal Cone Photoreceptor Cells/physiology
  • Retinal Cone Photoreceptor Cells/ultrastructure
  • Zebrafish/embryology
  • Zebrafish/metabolism*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
  • Zebrafish Proteins/pharmacology
  • Zebrafish Proteins/physiology*
PubMed
19384852 Full text @ Dev. Dyn.
Abstract
Kinesin 2 family members are involved in transport along ciliary microtubules. In Caenorhabditis elegans channel cilia, kinesin II and OSM-3 cooperate along microtubule doublets of the axoneme middle segment, whereas OSM-3 alone works on microtubule singlets to elongate the distal segment. Among sensory cilia, vertebrate photoreceptors share a similar axonemal structure with C. elegans channel cilia, and deficiency in either kinesin II or KIF17, the homologue of OSM-3, results in disruption of photoreceptor organization. However, direct comparison of the two effects is confounded by the use of different species and knockdown strategies in prior studies. Here, we directly compare the effects of dominant-negative kinesin II and KIF17 expression in zebrafish cone photoreceptors. Our data indicate that dominant-negative kinesin II disrupts function at the level of the inner segment and synaptic terminal and results in cell death. In contrast, dominant-negative KIF17 has no obvious effect on inner segment or synaptic organization but has an immediate impact on outer segment assembly.
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