C. elegans can detect a large number of chemicals using a small number of chemosensory neurons. Most of these chemosensory neurons are in bilaterally symmetric pairs, with one neuron on the left and one on the right side of the animal. Many candidate seven-transmembrane chemosensory receptors are expressed in these neurons, usually on both sides. One exception to this rule is the candidate odorant receptor
str-2. Surprisingly, we found that while
str-2 is expressed in the bilaterally "symmetric" AWC olfactory neurons, in half of the animals it is expressed only in AWCL and in half of the animals only in AWCR. The reasons for this asymmetry are mysterious; perhaps left and right neurons express different repertoires of receptors to increase the spectrum of odorants detected. To ask what genes are required for establishing and maintaining this asymmetry, we have examined
str-2::GFP reporter gene expression in several different mutant backgrounds. We have found that
str-2 asymmetry is disrupted in mutants that are likely to have less neuronal activity. For example, a gain-of-function mutation in the
egl-2 K+ potassium channel and a loss of function mutation in the
unc-36 Ca+ channel subunit, (as well as in the
unc-2 Ca+ channel subunit, see A. Sagasti abstract) cause
str-2 to be expressed in both AWCL and AWCR. Mutations in the cyclic nucleotide-gated
tax-2/4 channel can also disrupt
str-2 asymmetry, although to a lesser extent than
egl-2,
unc-2 and
unc-36 mutations. The axons of AWCL and AWCR contact one another and AWCR makes two synapses onto AWCL. However, we found that several genes required for synaptic transmission don't appear to be required for
str-2 asymmetry. Mutations in the CaMKII homolog,
unc-43, can disrupt
str-2 asymmetry. In an
unc-43(lf) background,
str-2::GFP is expressed in both AWC cells, while in an
unc-43(gf) background,
str-2::GFP is usually off in both cells. Our provisional model is that low Ca++ and subsequent low CaMKII activity in one AWC leads to
str-2 expression in that cell but not the other. We have also asked whether the STR-2 receptor itself can play a role in its own expression. Using the
odr-3 promoter, which drives expression in both AWC cells, we misexpressed the
str-2 cDNA and looked at its effect on
str-2::GFP expression. Driving STR-2 expression with this promoter can lead to misregulation of the
str-2::GFP reporter, with expression sometimes in both cells or sometimes in neither cell. This provocative result suggests a new role for odorant receptors in regulating their own expression. We thank D. Weinshenker, D. Reiner and J. Thomas for kindly providing the
egl-2 and
unc-43 strains. 1. D Weinshenker and JH Thomas, West Coast Worm Meeting 1996 Abstract#33. 2. DJ Reiner, H Tian, JH Thomas, WBG 14(4):73 (Oct. 1, 1996).