We are interested in understanding how the functions
of chemosensory neurons are specified during development.
What molecular instructions determine neuron identity?
How do sister-neurons adopt different fates? To address
these questions, we have identified and characterized
C elegans mutants defective in sensory neuron development.
Our approach was to mark particular chemosensory neurons
in vivo using green fluorescent protein (GFP) expressed
under the control of chemsensory neuron-specific promoters.
We have carried out screens using promoters specific for
either the AWA neurons, which sense a subset of volatile
attractants, or the polymodal ASH neurons. Strains of
worms with these GFP constructs were mutagenized, and
mutants showing aberrant maker expression were isolated.
From these screens, we isolated four phenotypic classes
of mutants: mutants in which expression of the marker::GFP
construct was faint or absent, mutants with ectopic expression,
mutants with cell position defects, and mutants with axon
or dendrite defects. Ten mutants have been isolated which
show faint marker expression'in AWA or ASH, and many also
show defects in neuronal function. Some of these mutants
identified known transcriptional regulators.
We also isolated mutants with ectopic neuronal expression
of AWA markers. One of these mutants, sns-3(oylO) (defects
in sensory neurons specification),
was the focus of my talk. We have isolated three mutants,
snd- 1, snc12, and snc13 (sensory
neuron defective) with abnormal chemsensory
cell positioning. In addition, we have isolated four mutants
with abnormal axons and/or dendrites.
We hope that by identifying and characterizing the mutants
from this screen, we will gain an understanding of how
the functions of the chemosensory neurons are specified
during development.
