We are interested in understanding how the diverse functions of chemosensory neurons are specified during development. To address this question, we have identified and characterized mutants defective in sensory neuron development. We expressed GFP specifically in the AWA neurons, which sense a subset of volatile attractants. Worms carrying this GFP construct were mutagenized, and mutants showing aberrant marker expression were identified. One mutant, previously referred to as
sns-3(
oy10) , shows ectopic expression of the AWA marker
odr-7::GFP in an additional pair of neurons. These neurons also express ODR-7 protein and other AWA markers including
odr-10::GFP and
gpa-5::GFP . The ciliary morphology of these neurons resembles that of AWA as well. The ectopically expressing neuron is in the correct position to be AWA's lineal sister ASG. Indeed, preliminary evidence suggests that in
sns-3(
oy10) animals, expression of the ASG marker
unc-30::GFP is frequently lost. This suggests that in
sns-3 mutants, ASG has been transformed into AWA. This perturbation of cell fate seems to be specific for the AWA/ASG lineage in the head. We have used markers to examine the fate of other head neurons including AWB, AWC, ASH, AFD, and AIY. While some of these neurons show minor abnormalities, none are perturbed to the same degree as AWA/ASG. We have cloned
sns-3(
oy10) and found that it is an allele of
unc-130 , a forkhead homolog previously cloned by Nash and Culotti.
unc-130 has distal tip cell migration defects similar to defects seen in
unc-5 ,
unc-6 , and
unc-40 mutants. We found no changes in AWA/ASG cell fate in these other mutants.
unc-130(
oy10) has a missense mutation in a conserved residue of the forkhead domain. We will be examining additional
unc-130 alleles generously provided by Nash and Culotti, to determine the extent of their AWA/ASG defects. Preliminary evidence indicates that
unc-130 is not expressed in AWA or ASG in adults; however, it does show broad embryonic expression which we are currently investigating. These results indicate that mutation of a forkhead homolog results in a cell fate conversion, in which ASG adopts an AWA-like cell fate. Further experiments are underway to test this model.