Behavioral Neurogenetic Studies of a Circadian Clock in Drosophila melanogaster

Citation

Orr, Dominic Ping-Yim (1982) Behavioral Neurogenetic Studies of a Circadian Clock in Drosophila melanogaster. Dissertation (Ph.D.), California Institute of Technology. doi:10.7907/wp4e-5054. https://resolver.caltech.edu/CaltechTHESIS:10222019-143344602

Abstract

The circadian clock controlling the locomotor activity of the adult fruitfly, Drosophila melanogaster, is studied in one wild-type and five clock mutant strains. Locomotive activity of individual flies are monitored using arrays of infra-red beams and detectors. It is found that the temperature compensation mechanism is intact in the mutants And and Clk^K06, is slightly defective in the mutant per^s and is grossly defective in the mutants per^l1 and per^l2. In the per^s and per^l1 mutants, this defect is enhanced when both eyes and major parts of both optic lobes are eliminated by a genetic mutation (sine oculus). The inter-individual variation of periods in a strain is found to increase much more than linearly with the average period of the same strain. The interaction between the And and the per loci and that between the And and Clk^K06 loci are found to be either very weak or non-existent (effects of mutations additive), whereas the interactions among the various alleles in the per locus are found to be strong (effects of mutations non-additive).

Ten 'Phase Resetting Curves' (PRC) obtained with saturating light pulses for six strains of flies at various temperatures are presented. All the ten cases exhibit basically 'type-1' resetting behavior (average slope = 1). Comparisons of the PRC's for per^s, per^l1 and wild-type at 17°C suggest that the mutations per^s and per^l1 change the period of the circadian clock by differentially shortening and lengthening, respectively, the duration of the 'subjective day' phase of the oscillation. Comparisons between the PRC's for per^s at 17°C, 22°C, and 25°C and comparison between the wild-type PRC's at 17°C and 22°C do not reveal major changes in the temporal structure of these two circadian clocks over the stated temperature ranges.

The responses of one wild-type and five mutant circadian clocks to sustained dim light of the range 5 x 10^-4 lux to 50 lux at 22°C are studied. In each strain, a critical 'window' of light intensity is found within which a variety of unstable clock features, including arrhythmia, are observed. The light intensity at which this critical window occurs in each of the mutant is 5 to 10 times lower than that in the wild-type. Responses from a ERG-defective mutant (norpA) are found to be qualitatively, but not quantitatively, similar to that of the wild-type. Responses from an eyeless and ocelli-less mutant (sine oculus) indicate that both period changes and arrhythmicity can be elicited by light in the absence of the compound eyes and ocelli. However, the sharp dependence of the occurences of these phenomena on light intensity is lost in this mutant.

Arguments are presented to suggest that none of the four mutations -- And, Clk^K06, per^s, and per^l1 -- cause changes of period by mimicking the effects of tonic light on the Drosophila circadian system.

The phase resetting curves (PRC) and the dim light responses described above are found to be incompatible with a particular model of the Velocity Response Curve (VRC) theory to inter-relate the phasic to tonic effects of light, in which the tonic effect of light is assumed to be the result of a summation of the effects of a contiguous series of single Light pulses, taking into account adaptation.

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