Ph.D., University of British Columba
Tel: (617) 552-6851
E-mail: swicks@bc.edu
Academic Profile
My laboratory is interested in the neurobiology of the chemosensory system.
We use molecular genetic, cell biological, and behavioral techniques to examine
the chemosensory system of the small nematode roundworm, Caenorhabditis
elegans. We are interested in two distinct aspects of this problem:
First, we wish to understand the development of the various cell types that
must interact during the formation of an intact sensory organ. How is the regulation
of this process organized? How is the developmental program executed? Many human
sensory disorders arise as a consequence of errors in the development and maintenance
of the sensory organ. Understanding the genetic control of this process in C.
elegans may help us diagnose and treat these human diseases. To study this
process in C. elegans we take advantage of an assay of structural integrity
of the adult organ. When animals are soaked in a lipophilic dye, the dye is
occluded from entering the animal at all points except the exposed tips of the
chemosensory neurons. The sensory neuronal membrane thus fluoresces with the
intercalated dye in a wild type animal. Mutations that perturb the development
of the sensory organ (the "amphid" in the worm) or the sensory neurons themselves,
lead to a dye-filling defective (Dyf) phenotype. We then clone
these mutations using modern molecular genetic and genomic technologies.
Second, we also wish to understand the functioning of the intact chemosensory
system. That is, once the chemosensory organ is in place, how does the animal
come to select one taste over another? This is a complex question that we try
to address in a couple of ways. First we execute genetic screens--based on direct
assays of behavior—for animals that can taste, but that have an
altered preference for one taste relative to another. Second, we turn to nematodes
in the natural world and try to understand the impact of strain variation on
taste preference. Not all isolates of C. elegans share the same taste
preferences, just as not all people share the same taste preferences. Since
all strains are raised under identical conditions in the lab, much of this strain
variation must be under a genetic locus of control. Each of these approaches
presents a unique set of challenges to the geneticist, and consequently we have
developed, and continue to refine, new methodologies and resources for forward
genetics in C. elegans.
Expression
of a gpa-15 G-alpha subunit-GFP fusion protein is restricted to a small
subset of chemosensory neurons in the head of C. elegans.
From Wicks et al. (2000).
These sensory neurons are required for responses to a variety of soluble
compounds, or tastes. We identify the molecular basis of mutations that alter
the development or function of the chemosensory apparatus in the worm model
system. Since the animals are small and transparent we can visualize and identify
individual neurons in the living animal. Furthermore, since many basic biological
processes are well conserved across the animal kingdom, we expect that much
of what we learn from the worm will aid our understanding of human diseases
and syndromes related to sensory system deficits.
Selected Publications
Blacque, O. E., Reardon, M. J., Li, C., McCarthy, J., Mahjoub, M. R., Ansley,
S. J., Badano, J. L., Mah, A. K., Beales, P. L., Davidson, W. S., Johnsen, R.
C., Audeh, M., Plasterk, R. H., Baillie, D. L., Katsanis, N., Quarmby, L. M.,
Wicks, S. R., Leroux, M. R. 2004. Loss of C. elegans BBS-7 and BBS-8
protein function results in cilia defects and compromised intraflagellar transport.
Genes & Development 18: 1630–1642.
Wicks, S. R., Yeh, R. T., Gish, W. R., Waterston, R. H., and Plasterk, R. H.
A. 2001. Rapid gene mapping in Caenorhabditis elegans using a high density
polymorphism map. Nature
Genetics 28: 160–164.
Siklos, S., Jasper, J. A., Wicks, S. R., and Rankin, C. H. 2000. Interactions
between an endogenous oscillator and response to tap in C. elegans. Psychobiology
28: 571–580.
Wicks, S. R., de Vries, C. J., van Luenen, H. G. A. M., and Plasterk, R. H.
A. 2000. CHE-3, a cytosolic dynien heavy chain isoform is required for sensory
neuron structure and function in C. elegans. Developmental Biology
221: 295–307.
Rankin, C. H., and Wicks, S. R. 2000. Mutations of the Caenorhabditis elegans
brain-specific inorganic phosphate transporter eat-4 affect habituation of the
tap-withdrawal response without affecting the response itself. Journal
of Neuroscience 20: 4337–4344.
Rankin, C. H., Gannon, T., and Wicks, S. R. 2000. A developmental analysis of
habituation kinetics in C. elegans. Developmental
Psychobiology 36: 261–270.
Wicks, S. R , and Rankin, C. H. 1997. The effects of tap withdrawal response
habituation on other withdrawal behaviors: The localization of habituation.
Behavioral Neuroscience 111(2): 342–353.
Wicks, S. R., and Rankin, C. H. 1996. The integration of antagonistic reflexes
revealed by laser ablation of identified neurons determines habituation kinetics
of the Caenorhabditis elegans tap withdrawal response. Journal of
Comparative Physiology A 179: 675–685.
Wicks, S. R., and Rankin, C. H. 1996. Recovery from habituation in Caenorhabditis
elegans is dependent on interstimulus interval and not habituation kinetics.
Behavioral Neuroscience 110(4): 840–844.
Wicks, S. R., Roehrig, C. J., and Rankin, C. H. 1996. A dynamic network simulation
of the nematode tap withdrawal circuit: predictions concerning synaptic function
using behavioral criteria. Journal
of Neuroscience 16(12): 4017–4031.
Wicks, S. R., and Rankin, C. H. 1995. Integration of mechanosensory stimuli
in Caenorhabditis elegans. Journal of Neuroscience 15(3): 2434–2444.
Racine, R. J., Moore, K. A., and Wicks, S. 1992. Activation of the NMDA receptor:
a correlate in the dentate gyrus field potential and its relationship to long-term
potentiation and kindling. Brain Research 556(2): 226–239.
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