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L I Lebedeva

Publications and source records attributed to L I Lebedeva.

At least 19 recordsLinked to original sources
PubMed2005

[Genetics of the cell cycle: adaptive modification of the cycB2g mutation expression in dividing cells of Drosophila melanogaster].

The effect of mutation CycB2g on mitosis in neural ganglia and imaginal disks was studied in third-instar larvae of Drosophila melanogaster. Chromosome condensation and segregation were shown to be impaired in dividing cells of mutant larvae. During the three-year period of maintenance of the mutation in heterozygote, frequencies of some defects decreased via cellular adaptive modification.

Animals↗
PubMed2004

[Key events in the cell cycle, their regulation and organization].

The review surveys the studies of molecular genetic mechanisms of the cell cycle control on various eukaryotic models. The major cell cycle phenomena are considered: (1) checkpoints and their role in preserving DNA integrity and fidelity of mitosis, (2) the cell oscillator model, and (3) the role of cyclins in timing of cell division and coordination of mitotic events. The main classes of regulatory proteins involved in the cell cycle are discussed in detail.

Cell Cycle↗
PubMed2004

[Genetic control of mitosis. Mast(v40) protein--an element of checkpoints system?].

The effect of the mastv40 mutation was studied using neural ganglion cells of third-instar larvae of Drosophila melanogaster. The distributions of the cells by the interphase nucleus diameter and by the distance between the sister chromosome sets in anaphase were analyzed. Three following types of defects induced by the mutation were described: (1) Monopolar mitosis or, in the case of bipolar mitosis, an abnormally short distance between the sister chromosome sets in anaphase and early telophase. We believe that these abnormalities are caused by damage of the start and (or) motor mechanisms of centrosome separation at the beginning and in the end of mitosis. (2) Lagging and bridging of chromosomes in anaphase and early telophase. These defects seem to be related to the disruption of functioning of mitotic spindle microtubules and (or) their defective attachment to the appropriate kinetochores. (3) Unlimited division of aneuploid and polyploid cells, which may be explained either by inactivation of the checkpoint system controlling the genome ploidy or by checkpoint adaptation. Taken collectively, our results and literature data suggest that the MAST protein is an element of the checkpoint system and that division of aneuploid and polyploid cells results from inactivation of the checkpoints.

Aneuploidy↗
PubMed2003

[Genetic control of mitosis. Premature beginning of telophase chromatin reorganization in cells of the Drosophila melanogaster strain with ff3 mutation].

The effect of cell cycle mutation ff3 on chromosome segregation was studied on fixed cells of neural ganglia. The cell distributions by diameter of interphase nuclei and by distance between sister chromatid sets were compared at anaphase and telophase. In the control wild-type strain Lausenne, the cell distribution by distance between sister chromatids in anaphase was similar to their distribution by nuclear size. The mean distance between segregating chromatids at anaphase (lcp) coincided with the mean diameter of interphase nuclei (dcp) and was 8.3 microns. Cells passed to telophase when chromatids were at least 10 microns apart. The mutant ff3 strain differed from the control strain Lausenne in cell distribution by interphase nuclear diameter and distance between sister chromatids in anaphase; the mean nuclear diameter and mean distance between segregating chromatids similarly increased to 9.3 microns. A specific feature of mitosis in mutant strain ff3 was a premature beginning of telophase chromatin reorganization. This caused the occurrence of cells with abnormally short (less then the interphase nuclear diameter) distance between sister chromatid sets in telophase but not in anaphase, as if these cells had passed from anaphase to telophase prematurely, during the chromatid movement toward poles in anaphase A.

Anaphase↗
PubMed2003

[Genetic control of mitosis: features of origin of sister chromatid sets in anaphase in Drosophila melanogaster mutant line aar(V158)].

The effect of mutation aarV158 on anaphase separation of chromatids was studied on fixed cells of neural ganglia of Drosophila melanogaster larvae. It was shown that mutation aarV158 causes three types of defective chromosome segregation manifested as (1) monopolar anaphase, (2) separation of chromatids to an abnormally short distance in anaphase, and (3) bridging and lagging of some chromatids or prolonged asynchronous separation of sister chromatid sets to the poles in anaphase. We believe that the former two types of defective segregation are caused by disturbed centrosome separation at the beginning of mitosis and the third type, by defects in chromatid separation during anaphase. During the two-year maintenance of the mutation in a heterozygous state, partial correction (adaptive modification) of the defects of type 1 and type 2 (but not type 3) occurred. The correction of type 1 and type 2 defects during adaptogenesis depended on the genotype: in heterozygotes and homozygotes, respectively type 1 and type 2 were preferentially corrected. The frequency of type 3 defects remained constant during the two-year period of maintenance of the mutation in a heterozygous state. However, in all variants of the experiment, their frequency decreased with increasing distance between the sister chromatid sets. In the cells that completed the previous division with abnormalities, the checkpoint system is supposed to effectively arrest the cell cycle in the subsequent division.

Anaphase↗
PubMed2001

[The effect of some mutations in the Trl gene on mitosis in embryonal and larval tissues and egg chamber morphology in Drosophila melanogaster].

A study was made of three insertional mutations (Trl13C, Trls2325, and TrlEP(3)3184) located in the second intron of the Trithorax-like (Trl) gene for the GAGA transcription factor (GAF). Their cytological effects were analyzed in oogenesis, early embryonic development, and in larval development (96-108 h) in cells of nervous ganglia and imaginal disks. Notwithstanding an interallelic difference in expression, all three P-element insertions proved to be dominant as far as the examined parameters were concerned. The most substantial defects were the formation of "granular" chromatin during the interphase and mitosis and high proportions of cells with hypercondensed chromatin (which were arrested at the G2/M boundary) and cells with abnormal chromosome segregation. A higher frequency of egg chambers with trophocytes defective in number and in chromatin condensation was observed in females carrying the mutant Trl gene. The defects were assumed to result from poor coordination of the chromosome and cell cycles and, including, the nuclear and centrosomal cycles in embryonic development and the cycles of chromosome condensation and spindle formation in cells of larval imaginal disks and nervous ganglia.

Animals↗
PubMed2000

[Genetic control of mitosis. Adaptive modifications of v158 mutation expression].

Cytogenetic parameters of mitosis were studied in the neural ganglions and imaginal disks of the third-instar Drosophila larvae of the marker lines ry506 and w; Cy/L; D/Sb; two wild-type lines Lausenne and Hikone-AW; and the v158 line mutant for the cell-cycle gene in the 85F locus. The control lines and their various tissues differ in a number of mitotic traits, which are believed to be the natural modifications of chromosome condensation and segregation and do not disturb homeostasis of the developing ry506, Lausenne, and Hikone-AW flies. Mutation v158 affects centromere disjunction. In imaginal disks, this results in arrest of either mitosis or anaphase initiation, whereas, in the neural ganglions, chromosomes integrate into a monopolar spindle at prophase and unipolar cells appear in anaphase. Different effects of the mutation in various tissues are assumed to be caused by different activity of the checkpoint system. When the mutation was maintained heterozygous for a long time, adaptive modification of its expression was observed. A comparison of the rates of two major and parallel mitotic processes, spindle formation and chromosome condensation, showed that adaptive modification can proceed via the adjustment of these rates.

Animals↗
PubMed1997

[Comparative dynamics of elimination of potential chromosome damage in mouse bone marrow cells after low and moderate doses of radiation].

Possible dynamics of the incidence, repair, and realization of potential chromosome aberrations (PAs) was examined by indirect methods based on cytogenetic analysis of radiation effects. PAs were characterized as chemical modifications of DNA responsible for the incidence of structural aberrations of chromosomes. We interpreted our data as providing evidence that two types of radiation-induced PAs, differing in repair rates, could occur in the exposed cells: quick- (short-term) and slow (long-term) repairing PAs. We showed that the PA spectrum gradually changed with an increase in radiation dose within the interval from 24 to 150 cGy. This process was paralleled by changes in the cell response and chromosome resistance to radiation. Short-term PAs were induced mainly by low radiation doses ranging from 24 to 75 cGy. Their incidence was associated with activation of the corresponding repair process. Further increase in radiation dose resulted in changes in the PA spectrum, and doses of 150 cGy induced predominantly long-term PAs with concomitant activation of the appropriate repair process. Induction of repair occurred in the dose intervals limited by lower and upper threshold doses, Dl and Du. In our experiments, short-term PAs were repaired when Dl < 24 cGy and 126 cGy < Du < < 150 cGy. Long-term PAs were repaired when 75 cGy < Dl < 99 cGy and Du > 150 cGy.

Animals↗
PubMed1996

[Possible mechanisms of the emergence of chromosome aberrations. VIII. Cytogenetic analysis of the dynamics of repair and occurrence of potential chromosome damage in bone marrow cells of gamma-irradiated mice].

The dynamics of mitosis delay and appearance of structural chromosomal aberrations (SCA) in relation to radiation dose and time after postradiation are studied. The results obtained suggest that potential DNA damage (PD)--chemical modifications responsible for SCA formation--induce a G2-block. According to this result, it was concluded that PD arose in 30, 80, 90, and 95% of cells at radiation doses of 9, 24, 51, and 75 cGy, respectively. In cycling cells, PD are either repaired or become SCA. If within the first hour after radiation, it was more probable that they would be repaired. The rate of PD repair decreased and the probability of SCA increased as the length of time after radiation increased. The probability of PD also depended on the separation rate of sister chromatids in mitosis. Radiation affects the rate of chromatid separation and, consequently, the occurrence of PD.

Animals↗
PubMed1993

[Possible mechanisms of the emergence of chromosome rearrangements. VI. Mitotic delay as a protective mechanism. Origin of spontaneous chromosome breaks].

It was proved by the investigation of the bone marrow cells and the culture of embryonic fibroblasts of mice, that experimental induction of chromosome breaks having such a distinctive feature as disposition of acentrics outside the equatorial plate at metaphase, results in reduction of the mitotic index and the radiation induced structural mutations frequency. Such disposition of acentrics--outside the equatorial plate--is typical for spontaneous chromosome breaks. It was suggested, that the process resulting in spontaneous chromosome breaks is a component of the protective mechanism, which is put into effect through the mitotic delay.

Animals↗
PubMed1991

[Possible mechanisms for occurrence of chromosomal restructuring. Interchromosomal contacts during metaphase and their role in chromosomal restructuring].

The influence of colchicine-hypotonic treatment on interchromosomal aberrations at metaphase was studied in bone marrow cells of BALB mice irradiated by X-rays within the dose range from 0.25 to 1.50 Gy. In was found that after 30 min treatment with 0.002% colchicine of cells dividing 10 h following irradiation, the frequency both of chromosomal exchanges and interchromosomal contacts decrease about 3.5 times, the amount of chromosomal breaks increasing. It is calculated from the data of this experiment that two breaks induced by irradiation, which were scored at the same K metaphase as independent ones, appeared to be associated with each other at high frequency through exchange in the absence of colchicine or hypotonic treatment. It is assumed that regions of interchromosomal contacts at native metaphase are the most radiation-sensitive zones of the genome preferentially involved in chromosomal aberrations of X-irradiated cells.

Animals↗
PubMed1988

[Possible mechanisms of the occurrence of chromosome restructurings. IV. Chromosome restructurings in spontaneous mutagenesis].

An attempt was undertaken to modify the spontaneous mutation process by varying its conditions in somatic cells of different species and tissues. The rate of chromosome aberrations and their types were studied in anaphase and metaphase. Under normal conditions, chromosome breaks were only found to occur. Breakage of chromosomes occurs during interphase, and as a result, acentric fragments are located outside the equatorial plate during metaphase. This process of chromosome breakage leads to elimination of some genetic material, without concomitant exchanges, and therefore, it has been named "elimination" process. Spontaneous chromosome mutagenesis manifesting itself at cytogenetic level was concluded to be an elimination process directed to elimination of a portion of chromatin from chromosomes. When the conditions of spontaneous mutagenesis are altered, in particular, by cardiovascular diseases in man, by partial inhibition of DNA repair in mice and pea cells, by transformation of Chinese hamster cells, upon ageing of pea seeds-qualitative changes in the chromosomal aberrations are registered, connected with the appearance of chromosome exchanges and acentric fragments situated within the equatorial plate during metaphase. These two types of chromosome aberrations are proposed to be considered as new criteria of pathology. A system of processes was suggested to exist, preventing the appearance of aberrations during mitosis, and it is supposed to be one of the most significant homeostatic systems.

Animals↗
PubMed1983

[Possible mechanisms of the origination of chromosomal restructurings. III. The role of chromosome association and isolation].

The kinetics of early appearance of chromosome breaks and exchanges (5-60 min after ionizing irradiation) in pea roots, in primary culture of embryonal fibroblasts of BALB mice and in chinese hamster cells BIId-ii-FAF-28 has been studied. It was found that chromosome resistance to irradiation increases during mitosis as fast as the process of chromosome isolation is advanced (the latter prevents the interchromosome and interchromatid contacts). From the outset of activation of sister chromatids isolation (i.e. from the end of prophase in pea and mouse cells, and from the beginning of prophase in hamster cells), the chromosomes "cease" to respond to irradiation. The prolongation of the period of isolation of sister chromatids in mouse cells by means of colchicine results in prolongation of the "insensitivity" period. A causal relationship between the chromosome isolation phenomenon and the increase in their radiosensitivity is supposed to exist. The importance of chromosome association and isolation in formation of chromosome breaks and exchanges is discussed.

Animals↗
PubMed1982

[Possible mechanisms of the occurrence of chromosome aberrations. I. Patterns in the occurrence of aberrations induced by ultraviolet irradiation].

The frequency of chromosome aberrations induced by UV light at wavelengths 254, 265, 280 and 302 using doses 2-10 J/m2 in the primary culture of mouse embryonic fibroblasts during the G1, S and G2 phases was studied at metaphase of the first mitosis. Two classes of chromosome aberrations were distinguished. These classes differ in the time intervals of the final establishment of the cell cycle. The aberrations of the class 1 emerge before the beginning of prometaphase (possibly, at interphase). Formation of the second class aberrations is completed during the metaphase. It is shown that the class 1 aberrations occur with almost the same rate in approx. 7% of cells, irrespective of the cell cycle, irradiation dose and wavelength. It is suggested that these aberrations arise as a result of indirect UV action on the chromosome structures; the mechanism of their emergence does not depend on DNA replication. The class 2 aberrations do not appear after UV irradiation during the post-DNA-synthetic G2 phase of the cell cycle. However, after UV treatment at the G1 or S periods, they represent the majority of aberrations and their rate increases almost monotonously with the radiation dose. The UV action spectrum for these aberrations coincides with the adsorption spectrum of thymidine and the action spectrum for DNA cross-links. Thus, it may be inferred that formation of DNA cross-links following thymine dimerization is the first step in formation of UV-induced aberrations of the class 2. The passage of cells through DNA replication is a very important step in the process of their emergence.

Acriflavine↗
PubMed1982

[Possible mechanisms of the occurrence of chromosome aberrations. II. The formation of aberrations induced by UV irradiation].

The report is concerned with one of possible mechanisms of emergence of chromosome aberrations after UV-irradiation of mammalian cells. The process is initiated by DNA cross-links following thymine dimerization, and is completed during mitosis. A model to account for formation of chromosome aberrations has been offered. It is compatible with the modern concept of a scaffolding model for metaphase chromosome structure in which the scaffold organizes DNA into loops along its length. The model predicts the importance of a process of mitotic chromosome isolation during aberration formation (in addition to the processes of DNA replication, reparation and chromosome association). Another feature of the model is an attempt to describe formation of aberrations under conditions of true DNA reparation.

Animals↗
PubMed1979

[Formation of structural chromosome mutations in metaphase of mitosis].

The rate of structural chromosome mutations at metaphase of the first mitosis was determined in culture of embrionic mouse fibroblasts after UV-irradiation during the S-period (lambda = 265 nm at an incident dose of 40 erg/mm2). It is established that the mutation rate is higher at late metaphase than at early metaphase. After the cell treatment with intercalating compounds (actinomycin D, acridine orange or ethidium bromide) at metaphase, the rate of UV-induced chromosome aberrations was decreased (about 2-fold). It is concluded from the results obtained that the majority of aberrations arise during metaphase after UV-irradiation in the process of DNA synthesis. After the cell treatment with o-methylhydroxylamine (OMHA) during the S-period the rate of structural mutations was the same at late and early metaphases. This rate was not affected by the caffeine treatment at metaphase; during this stage the acentric chromosome fragments lie outside the equatorial plate, which is an indication that the OMHA-induced aberrations, in contrast to the UV-induced aberrations, are formed before the beginning of metaphase, possibly during the interphase. It is suggested that the chromosome condensation during metaphase is of importance in the formation of structural mutations.

Acridine Orange↗