Electron microscopic and electron radioautographic study of cells in glandular hyperplasia and cancer of the endometrium

Peculiarities of the ultrastructure and RNA synthesis in the epithelial endometrial cells of nine patients with hyperplasia and the uterine cavity cancer have been studied by the electron-radioautographic method. Quantitative differences are revealed in the ultrastructures of the cells. Amplification of the nucleoli labelling and asynchronism of the RNA synthesis in the nucleoli with glandular hyperplasia and endometrial cancer are observed.     

Mobilization of the transposable element mdg4 by hybrid dysgenesis generates a family of unstable cut mutations in Drosophila melanogaster

Summary A family of unstable mutations at the cut locus in Drosophila melanogaster was obtained under the conditions of hybrid dysgenesis (Gerasimova 1981, 1982). The in situ hybridization experiments have shown that, in the original unstable ct ^MR2 mutation, the 7B region of the X chromosome (where cut is located) contains a mobile dispersed genetic element, mdg4. All other unstable ct mutations derived from ct ^MR2 including visible and lethal alleles and unstable ct ⁺ reversions, also contain mdg4 in the 7B region. The X chromosomes of the parent strain (wild type) do not contain mdg4 at all. All stable revertants derived from ct ^MR2, from other unstable ct mutations, or from ct lethals lost mdg4 from the 7B region. The ct ^MR2 X chromosome does not contain P-elements, although a few copies are present in the autosomes. The instability of the ct ^MR2./ct ^MR2 strain remained at a high level for 50 generations (1.5 years) and then rapidly decreased. A new cross with an MRh12/Cy strain (originally used for dysgenesis induction and containing a number of P-elements) increased the instability to a level exceeding the original one. The data strongly suggest that unstable ct mutations in our system are induced by transpositions of mdg4, possibly activated by P-elements.     

Investigations on the organization of genetic loci in Drosophila melanogaster: lethal mutations affecting 6-phosphogluconate dehydrogenase and their suppression.

Summary The molecular nature of lethal and semilethal mutations in the Pgd locus of D. melanogaster coding for 6-phosphogluconate dehydrogenase (6PGD) was studied. All the 11 mutations affect the structural gene of the Pgd locus: 3 semilethal mutations resulted in altered 6PGD molecules with decreased catalytic activities; the rest 8 lethals were null alleles characterized by mutant polypeptides capable of reacting with antisera against highly purified 6PGD.Null or low activity alleles for glucose-6-phosphate dehydrogenase induced by ethyl methanesulfonate were shown to be suppressors for the lethal mutations in the Pgd locus.A monocistronic type of organization of the Pgd locus is suggested taking into account the biochemical mechanism of suppression of the Pgd-lethals and their location in the structural gene coding for 6PGD.     

Plasmid transduction using the D3112DeltaH miniphage in Pseudomonas aeruginosa cells]

Plasmid DNA transduction with mini-D3112 delta H, deletion derivative of phage D3112, which lost the genes essential for phage growth but retained the sites required for transposition and packaging was studied. Unlike D3112, mini-D3112 delta H element can transduce plasmids and plasmid markers at frequencies of 10(-5)-10(-8) in rec+ cells of Pseudomonas aeruginosa. Plasmids R1162 and R388 of the size smaller than phage genome were transduced intact. Large plasmids, like RP4 and R151, were deleted under transduction. By this way, we isolated deletion derivatives of RP4. The smallest derivative pN2 contained a 4.5 kb fragment of RP4. Unlike the latter, pN2 plasmid had narrow host range and did not maintain in Escherichia coli cells.