[Heterochromatic ABO locus of the Drosophila melanogaster X chromosome overlaps with the region of localization of repeats, including mobile elements and Stellate genes]. / Geterokhromatinovyi lokus ABO X-khromosomy Drosophila melanogaster mozhet perekryvat'sia s rainom lokalizatsii povtvorov, vkliuchaiushchikh podvizhnye élementy i geny Stellate.

A loss of certain heterochromatic regions (ABO loci) of various chromosomes dramatically distorts the early embryo development in the progeny of females mutant for the abnormal oocyte (abo) gene, which is located in euchromatin of chromosome 2. One ABO locus (X-ABO) is in X-chromosomal heterochromatin distal of the nucleolus organizer. A cluster of the Stellate repeats is located in the same heterochromatin block. Deletions of various fragments from distal heterochromatin were tested for the effect on expression of the abo mutation. The X-ABO locus was assigned to X-chromosomal heterochromatin segment h26 and shown to include repeats consisting mostly of mobile elements and defective Stellate copies. A major part of the regular Stellate tandem repeats proved to be distal of the X-ABO locus.

[Trans-effect of modifiers on position-effect variegation in a set of euchromatin-heterochromatin rearrangements in Drosophila melanogaster]. / Issledovanie trans-deistviia modifikatorov na éffekt polozheniia v serii éu-geterokhromaticheskikh perestroek Drosophila melanogaster.

The effects of suppressors of position-effect variegation were studied in a set of euchromatin-heterochromatin rearrangements of the X chromosome accompanied by inactivation of the gene wapl. The rearrangements differed from one another in the size of the heterochromatic block adjacent to euchromatin, with the euchromatin-heterochromatin border remaining unchanged. In one rearrangement (r20), the position effect caused by a small block of adjacent heterochromatin may be determined by its interaction with the neighboring main heterochromatic region of the X chromosome. Chromosome 3 (the RT chromosome) was found to have a strong suppressing effect on all rearrangements, irrespective of the amount of heterochromatin adjacent to euchromatin. Su-var(3)9, a known suppressor of the position-effect variegation, had a considerably weaker suppressing effect. The RT chromosome had the strongest suppressing effect on the rearrangement r20.

The size and internal structure of a heterochromatic block determine its ability to induce position effect variegation in Drosophila melanogaster.

In the In(1LR)pn2a rearrangement, the 1A-2E euchromatic segment is transposed to the vicinity of X heterochromatin (Xh), resulting in position effect variegation (PEV) of the genes in the 2BE region. Practically the whole X-linked heterochromatin is situated adjacent to variegated euchromatic genes. Secondary rearrangements showing weakening or reversion of PEV were obtained by irradiation of the In(1LR)pn2a. These rearrangements demonstrate a positive correlation between the strength of PEV of the wapl locus and the sizes of the adjacent heterochromatic blocks carrying the centromere. The smallest PEV-inducing fragment consists of a block corresponding to approximately 10% of Xh and containing the entire XR, the centromere, and a very proximal portion of XL heterochromatin. Heterochromatic blocks retaining the entire XR near the 2E region, but lacking the centromere, show no PEV. Reversion of PEV was also observed as a result of an internal rearrangement of the Xh blocks where the centromere is moved away from the eu-heterochromatin boundary but the amount of X heterochromatin remaining adjacent to 2E is unchanged. We propose a primary role of the X pericentromeric region in PEV induction and an enhancing effect of the other blocks, positively correlated with their size.

Position-effect variegation in Drosophila melanogaster X chromosome inversion with a breakpoint in a satellite block and its suppression in a secondary rearrangement.

In(1LR)pn2a is a pericentric inversion with a euchromatic breakpoint in the 2E polytene region and a heterochromatic breakpoint in the right arm of the X chromosome. It is associated with position-effect variegation (PEV) of the pn, wapl, Pgd and other vital loci of the 2E region, which are relocated near the bulk of the X heterochromatin. Cytological analysis showed that the rearrangement brings the 1A-2E euchromatic segment directly into contact with a major portion of the h34 block, a heterochromatic region that is positively stained by the N-banding technique and contains the AAGAG satellite sequences. Molecular cloning revealed the presence of a new junction between euchromatin and AAGAG satellite sequences and demonstrated that the euchromatic breakpoint of In(1LR)pn2a lies in the vinculin gene. In the X ray-induced secondary rearrangement In(1LR)r30, consisting of a pericentric inversion superimposed on In(1LR)pn2a, the h34 material remains associated with the 2E region but is separated from the rest of the X heterochromatin. In this case, the pn, wapl and Pgd loci no longer variegate, suggesting that the satellite-containing h34 region is not able per se to induce detectable PEV on the adjacent euchromatic genes.

[X-ray-induced breaks in the X chromosomes in Drosophila lines of various radiosensitivities]. / Izuchenie indutsirovannykh rentgenovymi luchami razryvov X-khromosom v liniiakh drozofily s razlichnoi radiochuvstvitel'nost'iu.

The frequency of X-ray induced X-chromosome breaks has been studied in females of the line rad (2) 201G1 hypersensitive to radiation and in females of the control line selected from the same population. The frequency of X-chromosome breaks was judged based on the frequency of X0 males occurrence. Synergism of the effects of X-rays (at doses 0.1, 0.5 and 1.0 kr) and of hyperthermia (+37 degrees C, 5.5 hours) applied after irradiation served as an indirect evidence for the functioning of DNA repair systems. It is demonstrated that radiosensitivity of mature oocytes of the lines compared was equal and that hyperthermia applied after irradiation increased the latter effect in both lines. Young oocytes of the control line were radioresistant, and hyperthermia applied after irradiation enhanced its effect. Opposite to them, young oocytes of the rad line females were radiosensitive. They did not differ from mature oocytes in the frequency of X-chromosome losses. Synergism of the two factors (irradiation and hyperthermia) was not registered in young oocytes. On the basis of the results obtained, it may be concluded that radiosensitivity of young oocytes in the hypersensitive line is conditioned by the failure of DNA repair systems and that the rad (2) 201G1 gene may be considered, in relation to the genes controlling DNA repair, as a suppressor functioning selectively at a certain stage of oogenesis.