[Architecture of the X chromosome, expression of LIM kinase 1, and recombination in the agnostic mutants of Drosophila: a model of human Williams syndrome].

As the Human Genome and Drosophila Genome Projects were completed, it became clear that functions of human disease-associated genes may be elucidated by studying the phenotypic expression of mutations affecting their structural or functional homologs in Drosophila. Genomic diseases were identified as a new class of human disorders. Their cause is recombination, which takes place at gene-flanking duplicons to generate chromosome aberrations such as deletions, duplications, inversions, and translocations.

[Cyclic nucleotide phosphodiesterases in mutant lines of Drosophila melanogaster].

The activities of general phosphodiesterase and its Ca(2+)-calmodulin-independent from (PDE-1) were studied in strains mutant for the agnostic gene and in the strain Canton S. Enzyme activity was determined in males and homo- and hemizygous females of four strains. It was found that mutation at the agnostic gene resulted in increased PDE-1 activity.

Mutational analysis and genetic cloning of the agnostic locus, which regulates learning ability in Drosophila.

P-insertion mutations were obtained and localized by in situ methods at the agnostic gene (agn: 1-38.9; 11AB) in Drosophila. All agn mutants showed a wide spectrum of pleiotropic effects: an EMS-induced mutation of the agn-ts398 improved the ability to develop a conditioned defensive response and increased the activity of cAMP metabolic enzymes; spontaneous mutation of agnX1 showed morphological defects of the brain.

Genetic approaches to the study of memory in insects.

This article provides a short summary of studies carried out on mutant Drosophila with defects in learning ability, including our own experimental data on the role of the tryptophan oxygenase gene (this is a key enzyme, and is the first enzyme in the tryptophan-ommochrome metabolic pathway) in the inherited determination of learning ability and memory in the honey bee. A set of allelic mutations was used which inhibit the activity of this enzyme to different extents, resulting in the complete lack of kynurenines or particular levels of kynurenine deficiency in the mutant organisms. The effects of mutations at the snow locus (snow, s, snowlaranja, sla) on the dynamics of memory trace formation after single training sessions were studied in the honey bee and were related to the activity of the enzyme responsible for hydrolysis of cyclic nucleotides (phosphodiesterase).