[Transcription factors and the nuclear matrix]. / Faktory transkriptsii i iadernyi matriks.

Data on nuclear matrix-associated transcription factors are summarized. These transcription factors ensure the proper spatial arrangement of gene promoters and enhancers, interacting with DNA at matrix attachment regions (MARs) and with other nuclear matrix proteins. More than 50 individual proteins are considered and classified by the DNA-binding domain.

[Enzymatic activity of the nuclear matrix]. / Fermentativnye aktivnosti iadernogo matriksa.

The scope of the review is to illustrate the great diversity of enzymatic activities bound to the nuclear matrix. These data are usually summarized in terms of replication, transcription, DNA repair, etc. Such an approach is understandable; however, the great diversity of enzymes is thereby obscured. The review presents the data on enzymatic activities according to the International Enzyme Classification (EC) with the main emphasis on the enzymological aspects of the phenomena described. The enzymes represent almost all classes of enzymes discovered in the nuclear matrix: oxidoreductases, transferases, hydrolases, isomerases and ligases. The presence of ligases is supposed. Nuclear matrix enzymes form functional systems which provide the replication, transcription and regulation of gene expression, DNA repair, transduction of signals by the secondary messengers, antiviral defence, maintenance and modification of the nuclear matrix structure and recombination.

[DNA-protein interactions in CpG islands and DNAse I sensitive chromatin]. / Osobennosti DNK-belkovykh vzaimodeistvii v CPG-ostrovkakh i chuvstvitel'nom k DNKaze I khromatine.

DNA-protein interactions were studied in the chromatin preparations obtained according to different procedures by means of nucleoprotein-celite chromatography. Three discrete fractions dissociating in 1M, 2M and 3M NaCl were observed in all preparations. The 1M fraction prevails in DNaseI-sensitive chromatin and the 2M fraction--in the resistant. Chromatin solubilized by MspI restrictase (the active chromatin) contains the 1M and 3M fractions, one solubilized by AluI (inactive)--the 2M fraction. Distribution of the fractions is different in proliferating and quiescent cells.

[Effect of single-stranded breaks on the ultrastructural organization and cytochemistry of the chromatin in tumor cells]. / Vliianie odnonitevykh razryvov na ul'trastrukturnuiu organizatsiiu i tsitokhimiiu khromatina opukholevykh kletok.

Single-stranded DNA breaks in Zajdela's ascitic hepatoma and transformed hamster fibroblasts were caused by treating alive cells with 1% dimethylsulfoxide for 2 h or 100 micrograms/ml bleomycin for 5 min and tested by alkaline and neutral DNA elutions. Electron microscopy of thin sections revealed decompaction of the loosened approximately 25 nm globules within diffuse chromatin into thin fibrillar mesh while supranucleosomal structure of the compact chromatin remained untouched. The chromatin enhanced its affinity for cationic dyes and contrast agents. It is concluded that the diffuse chromatin possesses torsional stress of DNA superhelicity and its loosened subunits represent a form for its organization. They probably correspond to the functionally active (dynamic) nucleosomes which display destruction under DNA domain relaxation caused by one-strand breaks.

[Specificity of the interaction of carcinogenic and cytostatic agents with the elements of the genome at different levels of its organization]. / Spetsifichnost' vzaimodeistviia kantserogennykh i tsitostaticheskikh agentov s élementami genoma na raznykh urovniakh ego organizatsii.

The analysis of the literature permits drawing a conclusion that according to DNA binding site-specificity carcinogens and antitumour drugs can be divided into GC- and AT-binding compounds. When interacting with eucaryotic DNA such specificity leads to an increased binding of carcinogens and antitumour drugs to the repeat-rich DNA (satellite DNA, alpha-DNA, flanking regions of genes). It is supposed that specificity of the binding of chemical compounds on higher levels of genome organization (active and inactive chromatin, nuclear matrix-bound DNA) is also defined by the affinity of compounds to GC- or AT-rich repeats.

[Significance of inherited fragile sites in the occurrence of chromosome aberrations in tumor cells]. / Znachenie nasledstvennykh lomkikh uchastkov v vozniknovenii khromosomnykh aberratsii opukholevykh kletok.

The data on localization of heritable fragile sites and cellular oncogenes on individual human chromosomes involved in tumour-specific aberrations are summarized in the review. Only two fragile sites (8q22 and 11q13) out of eight ones, coinciding with breakage sites in such aberrations are the loci of cellular oncogenes (mos and bcl-1, respectively). Analysis of the data confirms the supposition that heritable fragile sites are predisposing factors for chromosomal rearrangements and in the end for development of the pathological processes.

[Chromosome aberrations and cellular antigens]. / Khromosomnye aberratsii i kletochnye antigeny.

A possible role of chromosomal abnormalities in activation of cellular oncogenes is discussed. Data about the types of chromosomal aberrations characteristic of tumours and of expression of oncogenes localized in aberrant chromosomes are compared. For some oncogenes (c-myc, c-myb, c-abl, c-fes, c-fms) a more or less distinct correlation is observed between certain types of chromosomal abnormalities and increase of oncogene expression. On the contrary, one cannot observe such correlation for other group of oncogenes (c-fos, c-ets, c-mos, c-erb-A-1, c-sis, c-src). Chromosomal aberrations are probably one of the mechanisms of cellular oncogene activation during the carcinogenesis.

[Reversible accumulation of double- and single-strand breaks of DNA during transition of cells into the quiescent stage]. / Obratimoe nakoplenie dvu- i odno-nitevykh razryvov DNK pri perekhode kletok c sostoianie pokoia.

The technique of neutral elution has been used to study DNA fragmentation in SV-40-transformed Hungarian hamster fibroblasts of 4/21 strain. Accumulation of DNA double-strand breaks was observed in growth-arrested cells. The breaks were repaired after the growth resumed. It is suggested that double-strand breaks are a sum of one-strand breaks.

[DNA and chromatin defects induced by thiophosphamide]. / Povrezhdeniia DNK i khromatina, indutsiruemye tiofosfamidom.

Treatment of mouse embryo fibroblasts with thio-TEPA (100 micrograms/ml) induced the formation of DNA interstrand cross-links after 10 hours and of DNA one-strand breaks after 20 hours. A short-term incubation of the cells with high concentrations of thio-TEPA (1 mg/ml, 30 min) resulted in a gradual increase of DNA cross-linking, which reached its maximal value after 4 hours of post-incubation. The cross-linking of DNA as well as the formation of DNA one-strand breaks was accompanied by a weakening of DNA-protein interactions in the chromatin. The prolonged existence of DNA and chromatin lesions is supposed to be an important step in the molecular mechanism of action of thio-TEPA.

[Repair of DNA injuries induced by thiophosphamide in embryonal fibroblasts of 101/H and CBA mice]. / Reparatsiia povrezhdenii DNK, indutsirovannykh tiofosfamidom v émbrional'nykh fibroblastakh myshei linii 101/H i CBA.

A study was made of changes in the molecular weight of one-strand fragments of DNA after a short-term treatment with thiophosphamide given in high concentrations of 101/H and CBA mouse cells. The data obtained indicate that DNA lesions induced by thiophosphamide occur and increase with time. It is assumed that the site of lesion is inter-strand cross-links of DNA. Mouse cells were disclosed to be able to repair the thiophosphamide-induced DNA lesions. Repair of DNA cross-links proceeds more effectively in 101/H mouse cells than in those of CBA mice.

[Repair of embichin-induced DNA damage in embryonal fibroblasts of 101/H and CBA mice]. / Reparatsiia povrezhdenii DNK, indutsirovannykh émbikhinom, v émbrional'nykh fibroblastakh myshei linii 101/H i CBA.

The changes in the molecular weight of DNA one-strand fragments were studied after a short-term incubation of 101/H and CBA mouse cells with embichin (nitrogen mustard). Unlike CBA mouse cells in which the repair of DNA lesions is completed after 24 hours, DNA in 101/H mouse cells was shown to be strongly fragmented. It is assumed that the deficiency of the repair of DNA lesions induced by embichin in 101H/ mouse cells is due to the deficiency of the last stage of excision repair, namely of the ligase reaction or to the uncoordinated pattern of the endonuclease and ligase reactions.

[Chromosome aberrations and molecular weight of single-stranded DNA fragments in embryonal fibroblasts of mouse strains 101/H and CBA]. / Khromosomnye aberratsii i molekuliarnaia massa odnonitevykh fragmentov DNK v émbrional'nykh fibroblastakh myshei linii 101/H i CBA.

Fibroblasts from 101/H mouse fetuses manifest a higher rate of spontaneous chromosome aberrations as compared to fibroblasts from CBA fetuses. The molecular weight of single-strand DNA fragments from 101/H mice was found to be lower than that in CBA mice. No differences were disclosed in the strength of the DNA-protein bond in the cell chromatin of both mouse strains. It is assumed that the alkaline-labile-sites in DNA may be the cause of chromosome aberrations. The possibility of using 101/H mice as a model of human chromosomal instability syndromes is discussed.

[101/H line mice, a possible model of human chromosomal instability diseases]. / Myshi linii 101/H--vozmozhnaia model' zabolevanii cheloveka s khromosomnoi nestabil'nost'iu.

Chromosome aberrations were studied in cells of embryo liver of 101/H and CBA mice following mutagenic treatment with the alkylating agent--thiophosphamide. Higher sensitivity of chromosomes to aberration induction was found in 101/H mice. After crossing thiophosphamide treated 101/H and CBA males to untreated 101/H and CBA females, the lowest output of dominant lethal mutations was found in the progeny of 101/H females. It is suggested that the 101/H mice are a possible model of inherited diseases with chromosomal instability.