Phototransduction Mutants of Drosophila Melanogaster

Abstract

One of the least understood problems in sensory physiology still remains the transduction process, i.e. the mechanism by which the reception of sensory stimuli is linked to ionic events in the receptor membrane. Several years ago we decided to approach the problem of transduction in visual receptors with the use of mutants, because it seemed to us that alternative approaches to the study of receptors were badly needed. The approach is based on the notion that the gene represents the ultimate unit of physiological function. Thus, a single-step mutation alters or removes a unit of function. Ideally this allows one to study the system in the absence of a single component at a time. It is hardly necessary to detail the success this approach has had in elucidating cellular functions at the microorganismal level. More recently, this approach has been applied to explore the mechanisms of photosynthesis (Levine, 1968), bacterial chemotaxis (Adler, 1969), and protozoan motility (Kung, 1971). The present study and other studies of a similar nature (Benzer, 1967; Ikeda and Kaplan, 1970; Heisenberg, 1971) represent attempts to extend the technique of induced mutation to the nervous system and to the behaviour it subserves. Of all the processes of the nervous system, the receptor mechanism appeared to us to be one of the more logical places to attempt to apply the potentially powerful technique of induced mutation. Unlike more central processes of the nervous system, the receptor process is not likely to be complicated by such problems as neuronal plasticity, multiple pathways, and modifications by the environment.

The erratum of this chapter is available at http://dx.doi.org/10.1007/978-1-4684-8231-7_33