Worm Breeder's Gazette 11(4): 107

These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.

Chemotaxis to Volatile Odorants

Cori Bargmann, Dean Jacobson and Bob Horvitz

C.  elegans will chemotax to bacteria, its food source, and to 
various attractive molecules.  The cells required for chemotaxis can 
be identified by killing cells with a laser and testing the behavior 
of the operated animals.  A group of chemosensory neurons (ASE, ADF, 
ASG, and ASI) is required for chemotaxis to several small water-
soluble molecules (cAMP, biotin, and Na+ and Cl- ions).  An 
overlapping but distinct group of chemosensory neurons is required for 
chemotaxis to lysine (ASE, ASG, ASI, and ASK).  All of these neurons 
have endings that are exposed to the environment through the opening 
of the amphid channel.
We have found that C.  elegans will also chemotax to low 
concentrations of many small volatile molecules, including alcohols, 
ketones, esters, and aromatic compounds.  The exposed neurons of the 
amphid channel are not required for these responses.  For example, 
chemotaxis to volatile odorants is normal in osm-3 mutants, in which 
the exposed amphid neurons have abnormal sensory cilia.  In addition, 
animals in which all of the exposed amphid neurons were killed (using 
a laser microbeam) responded normally to several volatile odorants.  
Similar experiments indicate that none of the other exposed 
chemosensory neurons (the phasmid and inner labial neurons) is 
required for responses to volatile odorants.
Chemotaxis to the volatile odorants benzaldehyde and butanone is 
impaired if the AWC neurons, also called the amphid wing cells, are 
killed.  The AWC neurons have endings that are associated with the 
amphid sensilla, but the AWC sensory endings are encased within the 
amphid sheath cell rather than being directly exposed to the 
environment.  Killing the AWC neurons does not affect chemotaxis to 
small water-soluble molecules (cAMP and so forth).
These results suggest that different types of sensory neurons 
recognize water soluble molecules and volatile odorants in C.  elegans.
These cell types may be analogous to the different neuron types that 
mediate taste and olfaction in vertebrates and in Drosophila.We are 
isolating and characterizing mutants that are defective in their 
abilities to chemotax to particular attractants.  Of 49 mutant strains 
that fail to chemotax to benzaldehyde, at least 12 are still able to 
chemotax to some other attractants.  The specificity of the defects in 
these mutants indicates that their inability to chemotax to some 
attractants is not a trivial consequence of uncoordination or sickness.
Mutations that lead to defects restricted to the response to 
volatile compounds are called odr (odorant response) mutations.  
Mutations in the odr-1 X gene (3 alleles) lead to strong defects in 
chemotaxis to many volatile odorants.  In serial electron micrographs, 
the AWC neurons in odr-1 animals appear to have stunted sensory 
endings.  Thus both laser experiments and mutant analysis implicate 
the AWC neurons in the response to volatile odorants.  The exposed 
amphid neurons are superficially normal (by EM) in odr-1 animals, 
consistent with the normal response of these animals to water-soluble 
Mutations in odr-2 V (3 alleles), odr-3 V (2 alleles), and odr-4 III 
(1 allele) each affect different subsets of the odorant responses.  
These mutants are being analyzed genetically, behaviorally, and 
structurally to determine the nature of their defects.  Little is 
known about the molecular nature of olfactory receptors in any animal. 
It is possible that some of these genes encode molecules involved in 
chemoreception and signal transduction in C.  elegans.