Mutant Sensory Cilia in the Nematode Caenorhabditis elegans

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Table of contents  -  Abstract  -   Introduction  -   Materials & Methods  -   Results  -   Discussion  -   References

Introduction

 Cilia and flagella are ubiquitous eukaryotic organelles that have been adapted for two seemingly unrelated functions, sensory transduction and cell motility. In the unicellular eukaryotes, Chlamydomonas and Paramecium, for example, they are used for swimming. Similarly, flagella propel the sperm of many animals and lower plants. Arrays of motile cilia line various epithelia, including the respiratory tracts, the oviducts, and the ventricles of the brain, where they propel fluid or particles along the surface.

Sensory cilia are found in the rod and cone cells of the eye, the hair cells of the ear, and the olfactory receptor neurons. In nematodes, cilia are found only in the nervous system where they are sensory receptors specialized for diverse modalities (Ward et al, 1975; Ware et al, 1975). Of the 118 classes of neurons in Caenorhabiditis elegans hermaphrodites, 24 classes have cilia (White et al, 1986).

 The common plan of both motile and sensory cilia is a membrane-bound cylinder of nine doublet microtubules that extend from a centriole. Many cilia have additional structures that adapt them to specific tasks. As they are biochemically complex structures and, in many cases, present in limited numbers, genetic studies have been helpful in understanding the assembly and function of cilia (Afzelius, 1981). In Chlamydamonas and Paramecium, genes coding for ciliary proteins have been identified by selecting for mutants with abnormal swimming (Luck, 1984; Kung et al, 1975). In humans, genetic disorders of ciliary motility produce a syndrome of male infertility and respiratory distress (Afzelius, 1976).

In C. elegans, several collections of mutants have been obtained by selecting for altered sensory behavior (Dusenbery et al, 1975; Hedgecock and Russell, 1975; Lewis and Hodgkin, 1977; Culotti and Russell, 1978; Chalfie and Sulston, 1981; Riddle et al, 1981; Hodgkin, 1983; and Trent et al, 1983). While some of these mutations affect the sensory organs themselves (Lewis and Hodgkin, 1977; Albert et al, 1981; Chalfie and Sulston, 1981; R. Ware, D. Dusenbery, D. Clark, M. Szalay, and R. Russell, personal communication), others presumably disrupt behavior at steps downstream of transduction.

Recently we found that certain sensory neurons in C. elegans accumulate fluorescein when living animals are placed in a solution of this dye (Hedgecock et al, 1985). In this paper, we show that these neurons are chemosensory and that dye uptake occurs through their exposed cilia. We have used this dye-filling technique to identify a subset of behavioral mutants with primary defects in sensory cilia or their support cells. These mutations both prevent dye uptake and disrupt sensory behaviors.


Adapted by Yusuf KARABEY for WORMATLAS, 2003