Our lab is interested in understanding how the fate and functions of chemosensory neurons are determined. We have been looking for factors involved in the determination of AWA and AWB sensory neuron fate. The strategy we used is to identify mutants that misexpress GFP driven by the AWA specific promoter
odr-7 , or the AWB specific promoter
str-1 . AWA :Mutants in which AWA specific expression is altered fall into two categories. One class of mutants shows reduced expression of
odr-7:: GFP in the AWA neurons. At least one of these mutations is in the
odr-7 gene.
odr-7 appears to be required for maintenance but not initiation of its own expression. Other mutants in this class are currently being further characterized. A second class includes a mutant that shows
odr-7:: GFP expression in only one of the bilaterally symmetric AWA cells. Preliminary experiments show that this mutant has defects in AWA mediated behavior, consistent with its possible involvement in AWA specification and function. Further characterization of these mutants is underway, as well as a continuing search for additional mutants. AWB : To date, we have screened more than 8000 haploid genomes using
str-1:: GFP to follow AWB fate. These screens have isolated three classes of mutants. One class shows reduced
str-1:: GFP expression. Among mutants in this class we isolated several alleles of
lim-4 . Recent work by Sagasti et al has elucidated its role in AWB specification. In a
lim-4 mutant, AWB is converted to AWC (Sagasti, Bargmann, pers. comm). We have also isolated two alleles of
sns-8 X, which appears to function downstream of
lim-4 . Recent evidence suggests that
sns-8 may have a role in the maintenance of AWB fate in adults. We have also found a mutant with ectopic
str-1 expression. 29% of
sns-9 II mutants have an ectopic
str-1 ::GFP expressing cell when reared at 25.5degC. This ectopic cell appears to have AWB-like cilia. In the third class of mutants
str-1 expression is seen variably in one, both or none of the AWB neurons. The cloning and characterization of
sns-8 ,
sns-9 , and of the other mutants isolated, should provide insight into how AWB fate is initiated, restricted and maintained.