On the basis of chiasma distributions along bivalents in human male meiosis, genetic were counted for several chromosomal segments. These estimates appeared to be lower than the lengths corresponding genetic lengths produced in the recombination analysis. When al so cytological distances and numbers of markers used in multilocus mapping were taken into account, the regression estimates of genetic lengths were shown to satisfactorily fit the observed values. This indicates that mitotic crossingover, genetic conversion, mutation and errors in allel's identification in addition to meiotic crossingover, appear to contribute to the observed genetic maps. It is suggested that these namely events, rather than the typing errors suggested by Morton (1991), seem observed over those predicted on the basis of chiasma counts.
The first intron of the mts1 gene, a gene which is selectively expressed in metastatic cells and in normal cells that are motile, was found to be highly homologous to the CD3 delta enhancer element. Because of the homology between the CD3 delta enhancer and the first intron of mts1, we analysed the first intron of the mts1 gene to determine whether it functions as a transcriptional regulatory element. Highly metastatic CSML-0 cells transfected with chloramphenicol acetyltransferase containing plasmids demonstrated the ability of the mts1 first intron to function as a positive regulatory element. In vitro footprinting analysis using extracts from CSML-0 cells (which express mts1 at low levels) of CSML-100 cells (which express mts1 at high levels) identified a protected 16 nucleotide element in the first intron of mts1, regardless of the extract used. However, in vivo footprinting analysis of the same region identified the protected 16 nucleotide fragment only in the mts1 intron from CSML-100 cells, not from CSML-0 cells. Differences in the methylation pattern of the mts1 gene in CSML-100 cells and CSML-0 cells are known to exist, and may in part be responsible for the mts1 footprinting differences observed in vivo from the different cells lines.
A review of research on genetic control of meiotic recombination is presented. The genes controlling different stages of meiotic recombination were revealed. Possible relationship of the gene products with the process of genetic recombination is under discussion.
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.
