Biomedical subjects

E M Gracheva

Publications and source records attributed to E M Gracheva.

5 recordsLinked to original sources

PubMed2000

["Mode for mutation" in the natural population of Drosophila melanogaster from Umani is caused by distribution of a hobo-induced inversion in the regulatory region of the yellow gene].

A mutation outburst of the yellow gene occurred in a Drosophila melanogaster population from the town of Uman' from 1982 to 1991 and was associated with the instability of several alleles. Molecular genetic analysis revealed a deletion variant of the hobo transposable element in the same site of the regulatory region of yellow in the mutant alleles and their derivatives. The outburst of the yellow-2 mutations was attributed to the spreading of the X chromosome, which contained an inversion of the yellow regulatory region, through the population. Reinversion resulted in the wild-type phenotype. Crossing lines carrying the inversion with laboratory line C(1)DX, ywf induced instability of the yellow alleles, which was associated with duplication or multiplication of a fragment of the yellow gene. Most derivative lines eventually became stable. The loss of instability was not associated with phenotypic changes; molecular genetic changes included a loss of the duplicated sequences or a deletion of the inverted regulatory region of the yellow gene.

Animals↗

PubMed2000

[Insulators and interaction between long-distance regulatory elements in higher eukaryotes].

Enhancers can activate a promoter located as far as several hundred kilobases away, which is specific for transcription regulation in higher eukaryotes. Notwithstanding the vast information accumulated on transcription regulation at various levels, the mechanism of long-distance enhancer-promoter interactions is still obscure. Modern views of insulators as elements modulating enhancer-promoter interactions are reviewed.

Enhancer Elements, Genetic↗

PubMed1999

[Isolation and genetic analysis of double hyperunstable systems in Drosophila melanogaster].

Hyperunstable mutations were described previously at the yellow locus of Drosophila melanogaster. These mutations are related to the insertion of the complex sequence containing two deleted copies of the P element at the termini and central unique regions from different sites of the X chromosome. In this work, double hyperunstable mutations at loci yellow and scute were obtained. These events were shown to occur from the inversion induced by the P elements located at the loci yellow and scute.

Alleles↗

PubMed1998

[Molecular analysis of a double hyperunstable system y(2ns)sc(me)].

Molecular analysis of hyperunstable mutations in the adjacent yellow and scute loci was performed in a Drosophila melanogaster strain y2ns scme obtained earlier. The y2ns scme combination originated from the original y+ns mutation associated with the insertion into the regulatory region of the yellow gene of a chimeric sequence flanked by deletion copies of the P element. The new combination of mutations resulted from an inversion between P-element copies located in the adjacent yellow and scute loci. The inversion was flanked by two P-element copies at one side and one copy at the other side. All three P-element copies had various internal deletions and, therefore, could not code for active transposase. An introduction of the delta (2-3) gene for transposase induced mutagenesis in the y2ns scme strain. Most mutations observed were associated with either excision of a single P-element copy or reinversion resulting from the recombination between the ends of P elements located in the yellow and scute genes. Genetic analysis showed that the alleles resulting from the recombination at a high frequency reverted to the original state.

Alleles↗

PubMed1998

[Mutation bursts of the yellow gene in a natural Drosophila melanogaster population is connected with insertion of the hobo transposon].

In 1981, a recurrent local burst of high mutability and high allele frequency of the yellow gene was recorded in the natural population of Drosophila melanogaster from Uman', Ukraine. A detailed genetic analysis showed that hypomorphic alleles y2 prevailed during the mutation burst. Mutations were strictly allele-specific and occurred only in two directions: from y2 to y+ and from y+ to y2. Alleles y2 isolated from the natural population differed in the degree of instability of mutant and wild-type derivatives, expression of the mutant phenotype, and complementation properties. In this work, the insertion nature of all unstable alleles derived from the natural population is confirmed by direct molecular methods. The mutation burst at the yellow locus is shown to result from insertion of a defective hobo copy. Six mutations y2 independently isolated from the natural population were caused by an insertion of hobo in the same site of the yellow regulatory region. The hobo copies were identical according to the restriction map. In three y2 alleles, the mutant phenotype was associated with inversion between hobo copies, one of which was located in the yellow locus and the other, in another unidentified region of the X chromosome. The remaining y2 alleles were associated with deletions that were located in the vicinity of the hobo insertion site and in the region of yellow enhancers.

Alleles↗