[Dynamics of neurodegenerative processes and lifespan under the action of Cerebral combined with other pharmaceuticals in Drosophila melanogaster mutants].

Effective influence of the drug Cerebral and its micro- and macrofractions on the mean lifespan and degenerative process dynamics of Drosophila melanogaster have been investigated. No dose--effect dependence was detected when different concentrations of Cerebral were used. The administration of Cerebral as a neuroactivating remedy combined with piracetam and verapamil was most effective, leading to an increase in the lifespan and a delay in the appearance of brain degenerative processes.

[Genetic analysis of Drosophila melanogaster chromosome 3 neurodegenerative mutants induced with ethyl methanesulfonate].

Neurodegeneration, a pathological state accompanied by brain neuronal necrosis and changes in behavior, has been described for many animal species. However, the genetic control and molecular mechanisms of this process are yet vague. A large collection of neurodegenerative mutants of a model object, Drosophila melanogaster, can enhance understanding of these mechanisms. In this work, we have demonstrated that genetically determined anatomical changes in Drosophila brain are accompanied by a decreased lifespan and deviations from the wild-type sexual behavior and locomotor activity. It has been found that the genes vacuous and loechrig are candidates for molecular genetic analysis in eight mutants from the collection.

[Chemically induced Drosophila melanogaster mutants with changes in brain structure]. / Khimicheski indutsirovannyi mutagenez u Drosophila melanogaster s tsel'iu polucheniia mutantov s ismeneniiami v strukture mozga.

Neurodegenerative human diseases are caused by nerve cell death and anatomical changes in some brain regions. Molecular genetic studies of Drosophila showed that this organism can serve as a valuable test-system for conserved mechanisms underlying human nervous system disorders. Analysis of brain functions is possible when the mutants with disturbed functions are available. In this study, we have developed a unique collection of Drosophila melanogaster mutants with morphological and neurodegenerative changes in brain structure, which were induced by chemical mutagens.

[Genetic analysis of X-chromosome neurodegenerative mutants of Drosophila melanogaster induced by ethyl methansulfonate and nitrosoethylurea]. / Geneticheskii analiz neirodegenerativnykh mutantov Drosophila melanogaster po X-khromosome, indutsirovannykh étilmetansul'fonatom i nitrozoétilmochevinoi.

In a series of Drosophila mutants with changes in the brain structure, some characters (reduced life span, behavioral changes, and neuronal loss in various brain regions) resemble symptoms observed in human patients with neurodegenerative diseases. In addition, similar specific phenotypes shared by different species suggest that common mechanisms underlie degeneration of their nerve cell. This study reports the results of a genetic analysis of new X-chromosome mutants with neurodegenerative changes in brain structure, which were induced by chemical mutagenesis. According to complementation test, all mutants were divided into three complementation groups, in which the life span and dynamics of neurodegenerative changes were studied. The life span of Drosophila melanogaster flies was found to depend on the state of their nervous system.

[Genomic variation of laboratory strains and natural populations of Drosophila melanogaster exposed to X-irradiation]. / Genomnaia izmenchivost' laboratornykh linii i prirodnykh populiatsii Drosophila melanogaster pri deistvii rentgenovskogo izlucheniia.

The spontaneous and X-ray-induced mutation rates and spectrums were estimated in laboratory strains and natural populations of Drosophila melanogaster from the Chernobyl meltdown area. Laboratory strains Oregon R and y2w alpha 4 were stable. In all natural populations, the spontaneous mutation rate was an order of magnitude higher (10(-3)) than in laboratory strains. Irradiation at a total dose of 3000 R was shown to induce genetic instability in the stable laboratory strain y2w alpha 4 and to increase the mutation rate and spectrum range in the unstable natural population P1. A high level of genetic instability was observed both in the first and second generations. Genetic analysis by means of classical genetic and molecular methods was performed; in crosses, a collection of spontaneous and induced mutants was used. The molecular genetic nature of mutations at the white and cut loci was analyzed by Southern blot-hybridization. Mutations at the white locus were shown to result both from transposition and recombination events; cut mutations were caused by deletions.

[Phenoloxidase in the ontogeny of Drosophila melanogaster]. / Fenoloksidaza v ontogeneze Drosophila melanogaster.

Electrophoretic spectrum of phenoloxidase was studied in 5 wild type and 17 mutant lines of D. melanogaster. Low-molecular alcohols (methanol, ethanol, and isopropanol) proved to be activators of the enzyme. Separate components of the phenoloxidase complex were activated by different agents. Electrophoretic spectrum of phenoloxidase was identical in larvae of 3rd age and 24-hour pupae. It consists of three fractions (A1, A2, and A3). Only the A1 fraction was seen on electrophoregrams of imago. No sex or age differences in phenoloxidase spectrum were observed during 25 days after birth. According to the A1 fraction polymorphism there were both normal and mutant genes coding for the A1 phenoloxidase subunit. The Dox-A1 gene that controls monophenoloxydase is located on the 2nd chromosome and is not linked with Dox-A2 and Dox-A3 genes coding for diphenoloxidases.