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[Clinical use of thrombopoietin (c-Mpl Ligand)].

INTRODUCTION: Results in clinical use of thrombopoietin have been published later than of other hematopoietic growth factors, because until recently the research was the least understood aspect of blood cell development. Reasons for this time gap were numerous, from inconvenient methods for measurement of thrombopoietin activity, to difficulties of its chemical purification. It is claimed recently that the understanding of platelet production has been profoundly advanced by the recombinant-gene synthesis and characterization of c-Mpl ligand (Megakaryocyte Growth and Development Factor), a substance which strongly enhances the proliferation of megakaryocytic line and the production of platelets. In this paper, some historical facts and biology of thrombopoietin are briefly discussed as well as the recent of the clinical use of thrombopoietin. THE HISTORY OF RESEARCH AND PRODUCTION OF THROMBOPOIETIN: The concept that the platelet production is underlying humoral regulation was first promoted by a group of Hungarian authors and they also named that humoral regulator--thrombopoietin. Further research followed in several countries including our own, and the initial studies proved that the serum of thrombocytopenic animals induced proliferation and maturation of megakaryocytic cell line and thrombocytosis in the peripheral blood of recipient animals. Later, when in vitro techniques were developed, it was shown that this humoral regulator has also a colony stimulating activity on megakaryocytic precursors. During the following two decades, studies of megakarycytopoiesis supported the hypothesis that two types of factors are involved in platelet production: early acting--megakaryocyte colony stimulating factors (Meg-CSF), and late acting--megakaryocyte potentiators, first of all thrombopoietin (TPO). However, extensive attempts on the purification of substances that either stimulate megakaryocyte development or augment platelet production failed to yield a homogeneous protein adequate for protein sequencing and cDNA cloning, the usual route which led to the production of other hematopoietic growth factors. Furthermore, a large number of other cytokines were described that possessed activity in various assays of megakaryocyte development. In spite of great number of accumulated data, it seemed in early 1990s that the production of a distinct, clinically useful lineage specific thrombopoietin will not be soon possible to achieve. The breakthrough occurred in 1994, when four groups of investigators published simultaneously their successful results on production of c-Mpl ligand, a substance which specifically binds to the Mpl receptors on megakaryocytes and has a very potent thrombocytopoietic effect. This production is based on genetic engineering and two companies (Kirin and Amgen) are already able to produce recombinant human thrombopoietin in large amounts, for clinical use. Although this substance is not commercially available yet, it passed the preclinical and clinical trials whose results are presented here. RESULTS OF THE PRECLINICAL TRIALS OF RECOMBINANT THROMBOPOIETIN: The chemical structure of human recombinant thrombopoietin (rTPO) is well defined, it is a glycoprotein consisting of 353 amino acids and molecular weight of 30 kD. The biologic actions of this molecule are in vitro: stimulation of megakaryocyte colony forming, endoreduplication of chromosomes and megakaryocyte maturation, and in vivo: increase of the number of progenitors and of megakaryocytes in the bone marrow, and an extensive elevation of platelet count in the peripheral blood 4-7 days after its application. Also, in synergism with other pluripotent cytokines, it can stimulate the proliferation of other progenitors including CD34+ stem cells. Based on these data it is considered that c-Mpl ligand is the main physiological humoral regulator of thrombocytopoiesis, having the biological actions both of MegCSF and TPO.

Animals↗

Experiments on blocking and unblocking of first meiotic metaphase in eggs of the parthenogenetic stick insect Carausius morosus Br. (Phasmida, Insecta).

The eggs of the parthenogenetic stick insect Carausius morosus, which remain arrested in first meiotic metaphase until oviposition, must be activated in order to develop. The activating agent is oxygen from the air, which enters the egg cell through the micropyle. An exposure shorter than one minute is sufficient to release the blockage. In non-activated (micropyle-less) eggs the first metaphase chromsomes either degenerate or change into an interphase nucleus. This nucleus polyploidizes by endoreduplication, and then either degenerates or multiplies by amitosis. Similarly more generations of nuclei may arise resulting in a chaotic development. These nuclei survive better in the anterior region of the egg. The question of whether the cytoplasmic factors which control nuclear behaviour, also operate in eggs of C. morosus is discussed.

Animals↗

Mechanisms of spontaneous and induced heteroploidization and polyploidization.

Mechanisms of heteroploidization and polyploidization were studied in tissue cultures, using various methods and cell lines. In untreated populations cells with different chromosome number are formed by mitotic non-disjunction. Mononuclear polyploid cells are formed by repeated DNA synthesis (endoreduplication) and polynuclear giant cells by postmitotic fusion of the daughter cells. These phenomena occur more frequently in cell populations treated with cystostatic drugs. Most polyploid cells are not viable.

Animals↗

Defective G1-S cell cycle checkpoint function sensitizes cells to microtubule inhibitor-induced apoptosis.

Defective cell cycle checkpoint function has been linked to enhanced sensitivity of tumor cells to certain genotoxic agents. To determine whether loss of the G1-S checkpoint function would sensitize tumor cells to microtubule inhibitor (MTI)-induced apoptosis, we examined the effect of the MTIs, Taxol and vincristine, on the cell cycle kinetics and survival of two isogenic cell lines, HCT116 p21+/+ and HCT116 p21-/-, which differ only at the p21 locus. p21-deficient cells displayed a dose-dependent, enhanced chemosensitivity to MTIs in both monolayer and soft agar assays as well as in mice xenograft tumors. The increased sensitivity of the p21-deficient cells to MTIs correlated with prolonged cyclin B1/Cdc2 activity and the occurrence of endoreduplication. Furthermore, sensitivity of p53-deficient cells to MTI-induced apoptosis was significantly reduced by induction of ectopic p21 protein. The results suggest that the status of G1-S checkpoint function in tumor cells may be an important determinant in the efficacy of MTIs used clinically.

Animals↗

Regulation of c-Myc and Max in megakaryocytic and monocytic-macrophagic differentiation of K562 cells induced by protein kinase C modifiers: c-Myc is down-regulated but does not inhibit differentiation.

We have studied the regulation and role of c-Myc and Max in the differentiation pathways induced in K562 cells by 12-O-tetradecanoyl phorbol-13 acetate (TPA) and staurosporine, an activator and inhibitor, respectively, of protein kinase C (PKC). We found that staurosporine induced megakaryocytic differentiation, as revealed by the cellular ultrastructure, platelet formation, and DNA endoreduplication. In contrast, TPA induced a differentiated phenotype that more closely resembled that of the monocyte-macrophage lineage. c-myc expression was down-regulated in K562 differentiated by both TPA and staurosporine, whereas max expression did not change in either case. Although PKC enzymatic activity was low in cells terminally differentiated with TPA and staurosporine, inhibition of PKC activity by itself did not induce c-myc down-regulation. We conclude that the c-myc gene is switched off as a consequence of the differentiation process triggered by these drugs in a manner independent from PKC. Ectopic overexpression of c-Myc in K562 cells did not affect the monocytic-macrophagic and megakaryocytic differentiation, indicating that c-Myc suppression is not required for these processes in K562. Similarly, both differentiation pathways were not affected by Max overexpression or by concomitant overexpression of c-Myc and Max. This result is in contrast with the inhibition of erythroid differentiation of K562 exerted by c-Myc, suggesting divergent roles for c-Myc/Max, depending on the differentiation pathway.

Basic Helix-Loop-Helix Leucine Zipper Transcriptio↗

Recurrent integration of human papillomaviruses 16, 45, and 67 near translocation breakpoints in new cervical cancer cell lines.

Progressive chromosomal changes and integration of human papillomavirus (HPV) sequences mark the development of invasive cervical cancer. Chromosomal localization of HPV integration is essential to the study of genomic regions involved in HPV-induced pathogenesis. Yet, the available information about HPV integration loci is still limited, especially with respect to different HPV types. We have established cell lines from five cervical cancers with HPV-16, HPV-45, and HPV-67. We have determined HPV integration sites and karyotype abnormalities by using the multicolor combined binary ratio-fluorescence in situ hybridization method (Tanke et al.) with 24 chromosome-specific paints in combination with full-length HPV DNA probes. All cell lines were cytogenetically abnormal, and exhibited numerical and structural chromosomal deviations. HPV sequences were integrated at various (segments of) chromosomes. Duplicate integration sites were seen in all multiploid cell lines, suggesting that viral integration had preceded chromosomal endoreduplication. HPV-16 was found near the t(3p14.1-14.3;14) breakpoint in cervical squamous cell carcinoma (CSCC)-7 and mainly in episomal form in CSCC-1. HPV-45 was integrated near 3q26-29 in cervical (adeno or adenosquamous) carcinoma (CC)-8 and near 1q21-23 as well as near the t(1q21;22q13) breakpoint in CC-10A and CC-10B variant lines. HPV-67 was localized near the breakpoint of t(3p23-26;13q22-31) in CC-11. Southern blot analysis showed that, except for CSCC-1, the physical state of HPV in the cell lines was the same as in the original tumor lesions. This set of six cervical cancer cell lines included three lines with HPV-45, a major non-Western high-risk HPV type, the first reported HPV-67-positive cell line, and two cell lines with integrated and episomal HPV-16 DNA, respectively. The novel combined binary ratio-fluorescence in situ hybridization technique enabled us to simultaneously map chromosomal rearrangements and HPV integration sites, thereby revealing recurrent integration near translocation junctions for all of these HPV types in the cell lines from three of the five primary tumors. The detection of multiple HPV integration sites at rearranged chromosomes at such high frequency in cervical cancer-derived cells may reflect events that are relevant to the development of cervical cancer.

Adult↗

[Cytogenetic characteristics of the growth of mouse ascitic strain L-5178].

The number of chromosomes in the cells of L-5178 ascites tumor vary from 38 to 46. The modal class consists of two cell lines with 43 and 44 chromosomes. The number of polyploid cells changes in the process of tumor growth from 11% within first 10 days after transplantation to 50% on the 21st-22en days. The tumor cell population manifests a number of metaphases with endoreduplication of chromosomes. The per cent of metaphases with diplochromosomes varies from 0.05% on the 7th day of tumor development to 5.0% on the 15th-17th day. L-5178 tumor cells are characterized by the presence of structurally changed chromosomes: the acrocentric chromosome with the secondary constriction, metacentric, and 2-3 small chromosomes.

Animals↗

[Theoretical models of chromatid exchange established after endoreplication analysi].

In endoreduplicating cells, two thirds of the chromatid exchanges observed after BrdU treatment are symetrical, like on the two elements of the diplochromosome. The other third seems to occur at random on one or the other element. Each double symetrical exchange would result from a single event occurring at the next to last cell cycle before the mitosis observed. The other exchanges would result from last events of the cycle. Thus the frequency of events would be the same at each cell generation. A theoretical model is proposed which explains the mechanism responsible for chromatid exchanges at the DNA level.

Acridines↗

[Genome multiplication in the trophoblasts and glandular epithelium of endometrium during embryo implantation and placentation of silver fox].

Dynamics of genome multiplication during establishment of interrelations between the trophoblast and the glandular epithelium of endometrium was studied in the course of placenta formation in the silver fox. Endometrium response on the embryo implantation exhibits some features of inflammation. In the course of placenta formation the trophoblast gains access to the endometrial glandular epithelium zone, while the endometrial blood vessels grow the other way into the expanding trophoblast zone. The trophoblast gradually replaces the whole epithelium and part of the stroma of the endometrium, closely adjoining the endometrial vessels but not disrupting them. Cytophometric DNA measurements in the trophoblast nuclei have shown that most of the nuclei are polyploid: predominantly 4c-64c, occasionally 128c and 256c. Polyploidy of the trophoblast may result from various types of polyploidizing mitoses. Cytophotometric DNA measurements in mitotic figures have revealed mitoses with DNA amounts equal to 4c (2n), 8c (4n), and 16c (8n), which indicates that trophoblast cells in the silver fox placenta are able to enter mitosis prior to the octaploid level. Higher degrees of polyploidy in the trophoblast cells may be achieved presumably by endoreduplication. In the silver fox polyploidization of uterine grandular epithelial cells during placentation occurs until the level of 8c. Thus, the tissue-specific response of the uterus to the implanting embryo is an active proliferation and polyploidization of the glandular epithelium, rather than formation of a population of polyploid decidual cells (i.e. connective tissue cells). Using the silver fox endotheliochorial placenta as an example, a regularity has been confirmed that cells of both maternal and fetal origin are polyploid in sites of their contact in placenta, which might be of protective significance in the contact of allogenic organisms.

Animals↗

Origins and complexes: the initiation of DNA replication.

Eukaryotic DNA is organized for replication as multiple replicons. DNA synthesis in each replicon is initiated at an origin of replication. In both budding yeast, Saccharomyces cerevisiae and fission yeast, Schizosaccharomyces pombe, origins contain specific sequences that are essential for initiation, although these differ significantly between the two yeasts with those of S. pombe being more complex then those of S. cerevisiae. However, it is not yet clear whether the replication origins of plants contain specific essential sequences or whether origin sites are determined by features of chromatin structure. In all eukaryotes there are several biochemical events that must take place before initiation can occur. These are the marking of the origins by the origin recognition complex (ORC), the loading onto the origins, in a series of steps, of origin activation factors including the MCM proteins, and the initial denaturation of the double helix to form a replication "bubble". Only then can the enzymes that actually initiate replication, primase and DNA polymerase-alpha, gain access to the template. In many cells this complex series of events occurs only once per cell cycle, ensuring that DNA is not re-replicated within one cycle. However, regulated re-replication of DNA within one cell cycle (DNA endoreduplication) is relatively common in plants, indicating that the "once-per-cycle" controls can be overridden.

Cell Cycle↗

Genome multiplication in the tertiary giant trophoblast cells in the course of their endovascular and interstitial invasion into the rat placenta decidua basalis.

Processes of invasion of the tertiary giant trophoblast cells (tGTCs) into the uterine wall in the course of implantation of the rat embryo at 10-15 days post coitum (dpc) were studied. Reproduction of tGTCs was evaluated using 3H-thymidine incorporation and cytophotometric measurement of the nuclear DNA content. 1. Patterns of trophoblast invasion. Two patterns of invasion were observed: endovascular (from 10 to 15 dpc) and interstitial (from 12 to 15 dpc), via extracellular matrix of endometrial stroma towards the central arterial channel. The both types of the tGTC invasion seem to take part in modification of the arterial wall. The tGTCs were shown to differentiate from cambial trophoblast cells of ectoplacental cone (EC) or junctional zone of placenta. 2. Peculiarities of reproduction of tGTCs. By the start of the endovascular and interstitial migration, tGTCs lose completely their capability for mitotic divisions and are found autoradiographically to stop incorporation of 3H-thymidine soon after beginning of their migration. Cytophotometric measurements of the nuclear DNA content have shown tGTCs to be polyploid. Their degree of ploidy is mainly 8-32c, which is by 1-2 classes of ploidy higher than that of the initial cambial cell populations of ectoplacental cone (EC) and junctional zone trophoblast cells (JTCs). Since the replication processes in tGTCs are limited, their polyploidization seems to occur within cambial populations of the trophoblast cells. The final genome multiplication cycles in the beginning of the tGTC invasion can be accomplished only via endoreduplication, i.e., with the complete elimination of the mitotic mechanism. The not too high level of tGTC ploidy, 8-32 c, probably does not prevent the tGTC deep invasion against the blood flow and through the extracellular matrix and may be of a protective significance in their interrelations with allogenic maternal tissues.

Animals↗

[Changes in cyclin expression during proliferation and differentiation of CD34(+) cells derived from fetal liver induced by thrombopoietin].

In order to elucidate the intrinsic mechanism underlying proliferation and differentiation of megakaryocytes during ontogenesis, CD34(+) cells were isolated from human fetal liver (FL) with a high-gradient magnetic sorting system (MACS) and were incubated in liquid suspension with 50 and 100 ng/ml of thrombopoietin (TPO) and in MegaCult(Tm) -C semi-solid culture system with 0, 12.5, 25, 50, 100, and 200 ng/ml of TPO. The cell number, colony number of CFU-Mk, platelet-associated antigen phenotype, and DNA ploidy of CD41(+) cells were examined from d 0 to d 12 in culture. The expression patterns of cyclins B1, D1, and D3 were also analyzed by using immunoblot and flow cytometry. TPO stimulated proliferation of CD34(+) cells of FL from 1 x 10(5)/ml to 13.12 +/-4.06 10(5)/ml with 95% of CD41a(+) cells and 3% of CD34(+) cells after 12 d of culture. Most of the megakaryocytes (MKs) derived from FL were in 2 N ploidy class, and few in 4 N ploidy class, but no megakaryocytes ploidy class was higher than 4 N. The effect of TPO on the formation of CFU-Mk colonies from FL derived CD34(+) cells is shown in a dose-response curve. The expression of cyclin B1 increased progressively and the high level of cyclin B1 was maintained in FL CD34(+) cells induced by TPO during 12 d of culture. A high level of cyclin B1 appeared on FL derived MKs of G1 phase at d 12. The expression of cy-of cyclins D1 and D3 gradually increased in FL CD34(+) cells, which was induced by TPO during the initial 6-day incubation. Afterwards, the level of cyclins D1 and D3 decreased progressively, particularly in MKs which were in G2+M phases. These data suggest that (1) TPO induced proliferation and differentiation of FL derived CD34(+) cells through upregulation of cyclin B1 in G2+M phases and cyclins D1 and D3 in all phases of cell cycle, and (2) Continuing high level of cyclin B1 and decreases of cyclins D1 and cyclin D3 on MKs in G2+M phases may contribute to a retardation of MK endoreduplication.

Antigens, CD34↗

[Effects of Methotrexat on the chromosomes of a human fetus in vivo (author's transl)].

A pregnant woman in the 17th week of gestation with Hodgkin's disease was treated with 50 mg Methotrexate i.v. on the 3 days preceeding therapeutic abortion. Cytogenetic studies on blood, brain, skin and lung of the fetus were performed. Slight structural aberrations such as gaps, chromatid breaks and accentric fragments were found in an average of 8,5% of the counted metaphases. The following drastic structural chromosome aberrations were found in 24,8% of all observed metaphases: 1) mitoses with stretched chromosomes, comparable with special segments (9,9%). 2) clumping of chromosomes in varying degrees (5,4%). 3) combinations of 1) and 2) (0,4%). 4) nuclear fragments (7,4%). 5) pulverized chromosomes (1,7%). Endoreduplications were found in 2%. The modal number was 46 with a rate of 50,1%, hypodiploids 46,3%, hyperdiploids and polyploids 3,6%. Karyotype: 46, XX.

Abortion, Therapeutic↗

Cellular bases of the antitumor activity of the novel taxane IDN 5109 (BAY59-8862) on hormone-refractory prostate cancer.

Taxane-based therapies appear to have a significant efficacy in clinical trials on hormone-refractory prostate carcinoma. In the present study, we investigated the cellular response of androgen-independent prostate carcinoma cell lines to the novel taxane IDN 5109 (BAY 59-8862) and evaluated its antitumor activity. In previous preclinical studies, this new paclitaxel (PTX) analogue was characterized by high tolerability and antitumor efficacy, ability to overcome multidrug resistance, and activity by oral administration. Upon treatment, DU145 and PC3 prostate carcinoma cell lines underwent a transient mitotic arrest. This was followed by G1 arrest and rapid occurrence of apoptosis in DU145 cells, whereas in PC3 cells, which are defective for the postmitotic checkpoint, a slow cell death was preceded by DNA endoreduplication. At the biochemical level, such events were associated with tubulin polymerization, activation of the mitosis-promoting factor, and phosphorylation of Bcl-X(L)/Bcl-2/Raf-1. In addition, IDN 5109 shared with PTX the ability to down-regulate the expression of the two potent angiogenic factors vascular endothelial growth factor and basic fibroblast growth factor. These findings indicated that IDN 5109 affected the same pathways involved in the cellular response to PTX and suggested that an antiangiogenic effect mediated by inhibition of paracrine stimulation of endothelial cells might contribute to the antitumor effect of both drugs. In in vivo experiments, the new taxane displayed a superior and more persistent effect compared with PTX against DU145 tumor xenografts. Such an effect was associated with pronounced reduction of the tumor microvessel density, superior to that achieved by PTX. These results support a potential therapeutic advantage of IDN 5109 over PTX against hormone-refractory prostate carcinoma.

Antineoplastic Agents↗

Genome multiplication of extravillous trophoblast cells in human placenta in the course of differentiation and invasion into endometrium and myometrium. I. Dynamics of polyploidization.

Polyploidization of the extravillous trophoblast (EVT) cells at different stages of differentiation and invasion into the uterine wall in human placenta has been studied. An increase in the ploidy level of EVT cells in the course of their differentiation within cell columns (CC) was shown. Stem cells were mainly diploid (86.2%); incidence of polyploid nuclei of highly proliferative cells of the proximal part of CC increased progressively. In the distal part of CC, where EVT cells did not divide mitotically, polyploid cells prevailed, with 58.0 and 3.5% nuclei being 4c and 8c, respectively. The highest percentage of polyploid cells was found in the population of EVT cells attached directly to the surface of the decidualized endometrium: percentage of tetraploid cells turned out to be 74.7% and the share of octaploid nuclei rose up to 4.9%; however, there appeared a few (0.3%) 16c cells. The majority of EVT cells invading the decidualized endometrium were polyploid, the share of octaploid and hexadecaploid cells rose up to 9.7 and 1.4%, respectively. On the other hand, the percentage of diploid cells also increased up to 29.2% as compared to EVT cells attached to decidua (20.0%). The same tendency proved to be even stronger in myometrium: the share of diploid EVT cells increased up to 46.0%, a prominent amount of tetraploid (45.1%) and highly polyploid (8c and 16c) cells retained in the EVT cell population (7.4 and 1.1%, respectively). Immunohistochemical staining of Ki-67 protein (MIB1), which labels cells held in the cell cycle, showed a high incidence of MIB1-positive stem cells (93.7%) and the EVT cells of the proximal part of CC (85.5%) characterized by high mitotic activity. A lower MIB1-positivity (43.2%) was found in the distal part of CC, whereas invasive EVT cells showed no MIB1-labeling. The presence of MIB1-positive nuclei in the distal part of CCs in the absence of mitoses, taken together with data on polyploidization of these cells, indicates their switch to the endoreduplication cycle. As a whole, the data obtained evidence that differentiation of EVT cells of the invasive pathway is accompanied by polyploidization. However, in a population of trophoblast cells capable of most profound invasion (up to myometrium), the proportion of diploid cells rose. These results suggest that the human cytotrophoblast invasion into the uterine wall requires an optimum, not the highest, ploidy level, whereas highly polyploid cells may form a subpopulation at the border between the maternal and fetal parts of placenta.

Cell Count↗

[Use of BrdU in the study of cell cycle in normal and abnormal subjects].

Chromosome modifications induced by BrdU allow a study of the cell division cycle during, at least, three consecutive generations. Among normal lymphocytes, the cell cycle varies in duration, but for the majority of cells, is a little shorter than twenty hours. In trisomy 21 individuals, the mean cell cycle is shorter, around 16 hours. In Fanconi's anemia, the cell cycle is slowed down and its duration is approximatively twice that of normal individuals. Endoreduplicating cells seem to have the cycle of longest duration.

Bromodeoxyuridine↗

[Elevated expression of argentophilic proteins from the nucleolar organizer regions in myocardium of patients with obstructive hypertrophic cardiomyopathy and mutations in p53 tumor suppressor gene].

Silver staining for nucleolar proteins was used to evaluate the ribosomal genes activity in cardiomyocytes (Cm) and fibroblast-like cells (FBS) of intraventricular septum, and other regions of the left ventricle. Specimens to be analysed were taken from 7 patients with idiopathic obstructive hypertrophic cardiomyopathy (OHCM). In this group the quantity of nucleoli and AgNORs, reflecting the transcriptional and processing level of pre-ribosomal RNA in all type of cells, was at least 2 and 3 times higher than in patients with essential hypertension and in healthy control, respectively. We suggest that nucleolar hypertrophy in patients with hypertrophic cardiomyopathies, inappropriate to hypertrophy in other pathological conditions, may be most probably of compensatory character, and this may be in part explained by nuclear hyperploidy and chromosomal endoreduplication. We have noted a marked heterogeneity in shape, size and quantity of nucleoli, and in AgNORs of FBC. Nuclei with modulated phenotype containing nucleoli of high activity were revealed. This article presents the first data on p53 mutation identification in patients with advanced OHCM.

Adult↗

[Effect of culture density on the polyteny degree of giant chromosomes in inbred lines and hybrids of Drosophila melanogaster].

The influence of culture density and genotype on the polyteny degree of giant chromosomes (PDC) in Drosophila melanogaster was investigated. The reliable depression of the polytene chromosomes endoreduplication function under increased culture density was revealed. The essential dependence of the PDC on the genotype was shown. Correlation between the PDC and the number of adaptive features was established. The certain parallelism between the increased heterosis effect on the number of quantitative characters and the superiority of the hybrids above the inbred lines on the PDC in conditions of high culture density was found out. The sex-dependent distinctions and maternal effect at the inheritance of the PDC in drosophila were shown.

Adaptation, Physiological↗