[Induction of unstable mutations in Drosophila melanogaster by microinjection of oncogenic virus DNA into polar embryonic plasm. Malignant effect of oncoviral DNA]. / Induktsiia nestabil'nykh mutatsii u Drosophila melanogaster mikroin''ektsei DNK onkogennykh virusov v poliarnuiu plazmu émbrionov. Maligniziruiushchii éffekt onkovirusnykh DNK.

We have demonstrated that the ability to induce benign neoplasms We have dominant mode of inheritance in Drosophila melanogaster is the specific feature of oncoviral DNAs. It is supposed that development of this type of neoplasms in Drosophila is connected with the changes in expression of protooncogenes in mutant genome: firstly, the genetic factors directing the development of neoplasms and Drosophila protooncogenes which shared the homology with v-src are localised in the same regions; secondly, there are structural rearrangements in c-src/fps (29A) protooncogene in mutant stocks which display the ability for neoplastic growth.

[Induction of unstable mutations in Drosophila melanogaster by microinjection of oncogenic virus DNA into the embryo polar plasma. Insertional nature of mutations]. / Induktsiia nestabil'nyukh mutatsii u Drosophila melanogaster mikroin"ektsiei DNK onkogennykh virusov v poliarnuiu plazmu émbrionov. Insertsionnaia priroda mutatsii.

We have demonstrated that mutations induced in Drosophila melanogaster by the microinjections of adenovirus Sa7 DNA in early embryos are of insertional nature. The role of insertional elements is played by the Drosophila transposons, but not by the virus DNA. The ability of oncoviral DNA to induce transpositions of mobile elements in recipient genome is the molecular basis of this system of genetic instability.

[Induction of unstable mutations in Drosophila melanogaster by microinjections of oncogenic virus DNA into the embryo polar plasma. Prolonged genetic instability of mutations at the lobe locus]. / Induktsiia nestabil'nykh mutatsii u Drosophila melanogaster mikroin"ektsiei DNK onkogennykh virusov v poliarnuiu plazmu émbrionov. Prodlennaia genet'icheskaia nestabil'nost' mutatsitii v lokuse lobe.

Mutations Lobe induced by the microinjections of RSV cDNA into Drosophila melanogaster early embryos are characterized by permanent genetic instability; the level of this instability is being changed in time. Based on the results of genetic analyses of Lobe mutations and molecular analysis of white and ADH mutations induced at high frequency in this system of gene instability, we supposed that unstable mutations which arose under the influence of retroviral cDNA are of the insertional nature.

INDUCTION OF UNSTABLE MUTATIONS IN DROSOPHILA MELANOGASTER BY THE MICROINJECTION OF ONCOGENIC VIRAL DNA INTO THE POLAR PLASM OF EMBRYOS: PROLONGED GENETIC INSTABILITY OF MUTATIONS AT THE LOBE LOCUS.

MUTATIONS IN THE LOBE LOCUS WERE PRODUCED BY MICROINJECTION OF RSV CDNA INTO EARLY EMBRYOS OF D. MELANOGASTER, AND SHOWED PROLONGED GENETIC INSTABILITY, THE EXTENT OF WHICH CHANGED SIGNIFICANTLY WITH TIME. GENETIC ANALYSIS OF LOBE-RSV MUTATIONS AND A MOLECULAR-BIOLOGICAL ANALYSIS OF STRUCTURAL REARRANGEMENTS IN THE W AND ADH LOCI, WHICH ARE FREQUENTLY MUTATED BY RETROVIRAL CDNA, SHOWED THAT THE MUTATIONS RESULTED FROM INSERTIONS ARISING IN THIS GENETIC INSTABILITY SYSTEM.

INDUCTION OF UNSTABLE MUTATIONS IN DROSOPHILA MELANOGASTER BY THE MICROINJECTION OF ONCOGENIC VIRAL DNA INTO THE POLAR PLASM OF EMBRYOS: THE INSERTIONAL NATURE OF THE MUTATIONS.

MUTATIONS INDUCED BY THE MICROINJECTION OF ADENOVIRUS SA7 DNA INTO THE POLAR PLASM OF DROSOPHILA MELANOGASTER EMBRYOS WERE SHOWN TO BE OF THE INSERTIONAL TYPE. THE INSERTED ELEMENTS RESPONSIBLE FOR THESE MUTATIONS WERE ENDOGENOUS TRANSPOSONS RATHER THAN VIRAL SEQUENCES. THUS, GENETIC INSTABILITY ACTIVATED BY ONCOVIRAL DNA RESULTED FROM THE ABILITY OF THESE DNA SEQUENCES TO INDUCE TRANSPOSITION OF MOBILE ELEMENTS IN THE RECIPIENT GENOMES.

[Characteristics of a frequently repetitive sequence family in the bull genome]. / Kharakteristika semeistva chasto povtoriaiushchikhsia posledovatel'nostei genoma byka.

The repeated sequences situated in 5'- and 3'-flanking regions of the bovine growth hormone gene were cloned and characterized. It was shown that they are related to a described before PstI-family of bovine repeats with a frequency of repetition about 10(5). PstI-repeats are found only in genomes of sheep and goats subfamily (Carpinae) and not found in DNA of other analysed vertebrate species. Repeats of this family are situated in the genome as a number of dispersed clusters, they have conservative structure and are alike by the frequency of repetition in the DNA of all organisms that contain them. The presence of sequences homologous to PstI-repeats are shown in bovine pituitary poly(A)+ cytoplasmic RNA by means of North-hybridization.

[A short repeat in the genome of the DNA sequences flanking bovine growth hormone genes]. / Umerennoe povtorenie v genome posledovatel'nostei DNK, okruzhaiushchikh gen gormona rosta byka.

The phage clones containing a gene coding for bovine growth hormone were isolated from a bovine genomic library. Comparison of the 5' and 3' regions flanking the bovine growth hormone gene by Southern blot hybridization revealed that they share homology. Screening the bovine genomic library by nick-translated DNA fragment from 5' flanking region leads to conclusion that this sequence is present in 0.1% of clones. Each analysed clone carrying the sequence contains some copies of it.

[The gene for bovine growth hormone is flanked by homologous sequences]. / Gen gormona rosta byka okruzhen gomologichnymi posledovatel'nostiami.

The gene coding for the bovine growth hormone was isolated from a lambda-phage library. The restriction map of the 3'-region (about 10 kb) was determined by restriction analysis and by Southern blot analysis. A comparison of the 5'- and 3'-flanking regions of the bovine growth hormone gene revealed some patches of homology.

Rearrangements of microinjected recombinant DNA in the genome of transgenic mice.

Previously, mouse zygotes were microinjected with the recombinant plasmid pMA3, which contains the Herpes simplex virus thymidine kinase gene attached to the promoter region of the Rous sarcoma virus (Gazaryan et al. 1984a). In the present work the pMA3 fragment with the flanking genomic sequences was isolated from the DNA of one transgenic Fo mouse by the "plasmid rescue" technique. The rescued plasmid (pMAR1) lacked all virus-specific sequences and retained only some pBR322 sequences. The flanking region at one end of the integrated pBR322-specific fragment contained a highly conserved mouse repetitive sequence. The possible mechanisms of rearrangement of foreign DNA in germ line cells are discussed.

[Cloning of the DNA fragment of a transgenic mouse containing an integrated recombinant plasmid]. / Klonirovanie fragmenta DNK transgennoi myshi, soderzhashchego integrirovannuiu rekombinantnuiu plazmidu.

The "plasmid rescue" method has been used to isolate the recombinant plasmid pMA3 fragment and flanking sequences from the transgenic mouse genome containing the fragment in integrated form. The "rescued" plasmid, pMAR1, lacks all virus sequences and retains only those regions of pBR322 that are responsible for the plasmid replication and Escherichia coli ampicillin resistance. The plasmid pMA3 deletion has occurred at its integration into the mouse genome after microinjection into the zygote. The integrated fragment of the plasmid is adjacent to the genome repeated sequence that is highly conservative in evolution.