title: Mutant sensory cilia in the nematode Caenorhabditis elegans.
abstract: Eight classes of chemosensory neurons in C. elegans fill with fluorescein when living animals are placed in a dye solution. Fluorescein enters the neurons through their exposed sensory cilia. Mutations in 14 genes prevent dye uptake and disrupt chemosensory behaviors. Each of these genes affects the ultrastructure of the chemosensory cilia or their accessory cells. In each case, the cilia are shorter or less exposed than normal, suggesting that dye contact is the principal factor under selection. Ten genes affect many or all of the sensory cilia in the head. The daf-19 (m86) mutation eliminates all cilia, leaving only occasional centrioles in the dendrites. The cilia in che-13 (e1805), osm-1 (p808), osm-5 (p813), and osm-6 (p811) mutants have normal transition zones and severely shortened axonemes. Doublet-microtubules, attached to the membrane by Y links, assemble ectopically proximal to the cilia in these mutants. The amphid cilia in che-11 (e1810) are irregular in diameter and contain dark ground material in the middle of the axonemes. Certain mechanocilia are also affected. The amphid cilia in che-10 (e1809) apparently degenerate, leaving dendrites with bulb-shaped endings filled with dark ground material. The mechanocilia lack striated rootlets. Cilia defects have also been found in che-2, che-3, and daf-10 mutants. The osm-3 (p802) mutation specifically eliminates the distal segment of the amphid cilia. Mutations in three genes affect sensillar support cells. The che-12 (e1812) mutation eliminates matrix material normally secreted by the amphid sheath cell. The che-14 (e1960) mutation disrupts the joining of the amphid sheath and socket cells to form the receptor channel. A similar defect has been observed in daf-6 mutants. Four additional genes affect specific classes of ciliated sensory neurons. The mec-1 and mec-8 (e398) mutations disrupt the fasciculation of the amphid cilia. The cat-6 (e1861) mutation disrupts the tubular bodies of the CEP mechanocilia. A cryophilic thermotaxis mutant, ttx-1 (p767), lacks fingers on the AFD dendrite, suggesting this neuron is thermosensory.
mesh_terms: D000818:Animals; D001522:Behavior, Animal / Q000502:physiology; D001833:Body Temperature Regulation; D002107:Caenorhabditis / Q000033:anatomy & histology / Q000235:genetics / Q000502:physiology*; D002628:Chemoreceptor Cells / Q000502:physiology / Q000648:ultrastructure; D002923:Cilia / Q000502:physiology / Q000648:ultrastructure; D016650:Fluorescein-5-isothiocyanate; D005452:Fluoresceins / Q000378:metabolism; D007473:Ion Channels / Q000502:physiology; D008465:Mechanoreceptors / Q000502:physiology / Q000648:ultrastructure; D008854:Microscopy, Electron; D009154:Mutation; D011984:Sensory Receptor Cells / Q000502:physiology* / Q000648:ultrastructure; D012726:Sexual Behavior, Animal / Q000502:physiology; D013861:Thiocyanates / Q000378:metabolism
chemical_list: D005452:Fluoresceins; D007473:Ion Channels; D013861:Thiocyanates; D016650:Fluorescein-5-isothiocyanate