1. [The mechanism of the effect of apterous56f mutation on the reproductive function of Drosophila melanogaster].
- Author
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Raushenbakh IIu, Gruntenko NE, Karpova eK, Adon'eva NV, Alekseev AA, Chentsova NA, Shumnaia LV, and Faddeeva NV
- Subjects
- Animals, Dopamine genetics, Dopamine metabolism, Dopamine Agents pharmacology, Drosophila Proteins metabolism, Drosophila melanogaster, Ecdysterone pharmacology, Female, Homeodomain Proteins metabolism, Juvenile Hormones genetics, Juvenile Hormones metabolism, LIM-Homeodomain Proteins, Levodopa pharmacology, Male, Oviposition drug effects, Reproduction drug effects, Reproduction genetics, Transcription Factors metabolism, Vitellogenesis drug effects, Drosophila Proteins genetics, Homeodomain Proteins genetics, Mutation, Oviposition genetics, Transcription Factors genetics, Vitellogenesis genetics
- Abstract
The effects of L-dihydroxyphenylalanine (L-DOPA) and 20-hydroxyecdysone (20E) were studied with respect to the content of dopamine (DA), intensity of the juvenile hormone (JH) degradation, and fecundity of the wildtype flies (Canton S) and JH-deficient apterous56f mutants (in young females, carrying this mutation, the levels of DA and 20E production were strongly increased). Fly feeding with L-DOPA proved to increase the level of DA in a dose-dependent manner and reduce JH degradation in 2-day-old females of both strains. Feeding with 20E produced the same effect. Treating the wild-type flies with 2.5 mg L-DOPA caused a 24-h delay in beginning of oviposition and reduction in fecundity throughout the experiment. An L-DOPA dose of 1 mg caused no such changes. An experimental increase in 20E titer led to reduced fecundity of the wild-type flies, though no delay in oviposition was observed. In mutant flies, an increase in DA and 20E levels accelerated beginning of oviposition and increased fecundity of young females, though the latter parameter was reduced in mature individuals. Thus, an increase in endogenous DA and 20E characteristic of young apterous56f females is assumed to be a compensatory response that leads to a higher JH titer and induction of vitellogenesis.
- Published
- 2006