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M D Golubovsky

Publications and source records attributed to M D Golubovsky.

8 recordsLinked to original sources
PubMed2003

Postzygotic diploidization of triploids as a source of unusual cases of mosaicism, chimerism and twinning.

Triploidy is one of the most frequent chromosomal errors responsible for reproduction failure. This paper encompasses, in one conceptual frame, four recent findings in reproduction biology: predominant dispermic origin of triploids, paternal centrosome inheritance, eccentric cleavage divisions of dispermic triploid zygotes and certain intricate cases of mosaicism/chimerism. It is argued that dispermic zygotes, in contrast to digynic ones, are characterized by cytogenetic phenomenon described here as postzygotic diploidization of triploids (PDT). PDT embraces three main developmental scenarios: (i) the maintenance of the triploid state accompanied by regular segregation of 2n cells and the 2n/3n mixoploid populations; (ii) immediate diploidization with elimination of an odd haploid set of chromosomes and regular appearance of 1n/2n, 2n/3n and other mixoploids and (iii) tripolar spindle formation leading to gross aneuploidy, cell death with occasional survival of 2n+1 or 2n+1+1 trisomics and uniparental disomics. According to the PDT concept, a trisomy and disomy might occur due to generalized karyotype instability of dispermic triploids. PDT may provide a natural explanation for the regular appearance of 2n homozygous androgenic moles, various 2n/3n, 2n/2n molar/twin complexes without necessitating the concept of the 'empty' oocyte fertilization. Convincing evidence for a reservoir of anuclear oocytes does not exist. Peculiar implications are expected in the case of two rounds of diploidizations or involvement of triploid cell derivatives in the twinning process. Cryptic mosaic/chimeras and unusual twins intermediate between monozygotic (MZ) and dizygotic (DZ) are expected. Thus, PDT could have an explanation for the broad spectrum of odd reproductive cytogenetic events and might provide additional alternatives and definite predictions.

Chimera↗
PubMed2001

Terminal retrotransposons activate a subtelomeric white transgene at the 2L telomere in Drosophila.

Genetically marked P elements inserted into the subtelomeric satellites of Drosophila show repression and variegation of the reporter gene. One such white+ reporter, inserted between the subtelomeric satellite and the terminal HeT-A array in the left arm of chromosome 2 (2L), is sensitive to its context; changes in the structure of the telomere region can be identified by changes in eye color. Addition of HeT-A or TART elements to the 2L terminus increases w+ expression, and loss of sequence from the end decreases expression. This indicates that the telomeric retrotransposons in Drosophila have an activating influence on the repressed subterminal reporter gene. Changes in eye color due to altered expression of the transgene also allow the detection of interactions between homologous telomeres. The 2L arms that terminate in long HeT-A/TART arrays showed increased expression of the subterminal w+ transgene when the terminal repeats on the homologue are absent or markedly shorter. We propose that the chromatin structure of the terminal HeT-A/TART array and the activity of a putative promoter/enhancer element on HeT-A are affected by telomeric interactions. Such trans-activation may reflect control over HeT-A transcription and, thus, transposition activity.

Animals↗
PubMed2000

hobo-induced rearrangements are responsible for mutation bursts at the yellow locus in a natural population of Drosophila melanogaster.

In 1981 recurrent local bursts of mutability of the yellow gene were observed in a natural population of Drosophila melanogaster from Uman' (Ukraine). A series of y2-like mutations in the yellow gene were recovered during the period 1982 to 1991. Most of the mutants display the y2-phenotype, i.e. mutant yellow color of wings and body cuticle. Ninety-nine y2 mutants were shown to be generated by an inversion that occurred between two hobo elements, one located 129 bp from the start site of yellow transcription, and the other in the distal telomere region. The y2 phenotype was caused by the separation of the body and wing enhancers from the transcription unit. Many of the y2-like alleles were highly unstable and reverted to y+, which again, gave rise to y2-like mutants. We found that the y2-->y+-->y2 transitions were generated by repeated inversions between the two hobo elements mentioned. The y2 and y+ alleles lost their instability after deletion of the hobo element present at the tip of the X chromosome.

Alleles↗
PubMed1982

Mutability studies in two Drosophila melanogaster isogenic stocks, endemic for C picornavirus and virus-free.

A virus-free Drosophila stock was obtained by outer disinfection of eggs from DCV-contaminated females. The healthy flies exhibited 3 times less lethal mutations on the X chromosome than did the diseased flies. In addition, on X and 2nd chromosomes, the mutability of the infected males was 2-3 times lower than that of the infected females. The natural viruses of Drosophila are partially responsible for the rate of mutations occurring in the wild populations of this insect.

Animals↗
PubMed1977

Genetic instability in Drosophila melanogaster: putative multiple insertion mutants at the singed bristle locus.

A series of eleven independent mutants at the X chromosome singed bristle (sn) locus of Drosophila melanogaster is described. All mutants descend from flies caught in the wild and bred in the laboratory. On the basis of their inordinately high spontaneous mutation frequency, ten of the mutants are classified as putative insertion mutants. Reversions to wild type occur at frequencies of 10(-4)-10(-3). Some reversions appear to be losses of the inserted element, others appear (by analogy with prokaryotes) to be changes in the orientation of the inserted elements. Consistent with the insertion hypothesis, some sn mutants generate what are interpreted to be deletions at the sn locus. In their mutational properties, the sn mutants are analogous to insertion sequence (IS) elements and bacteriophage Mu of Escherichia coli, but the precise nature of the insertion remains unknown.

Alleles↗