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PubMed1994

[The resistance of Amoeba proteus amebae with different levels of nuclear DNA to the action of high temperature and ethyl alcohol].

Thermotolerance and resistance to ethyl alcohol were investigated in Amoeba proteus of polyploid series. Thermoresistance of these amoebae was determined by measuring the mean time of survival at the lethal temperature (43 degrees C). The resistance to ethyl alcohol was estimated by the mean percentage of individuals that survived following a 5-minute treatment with 7.5% ethyl alcohol. Neither thermotolerance, nor ethyl alcohol resistance were found to depend on the amount of nuclear DNA. It was also established that colchicine did not induce a hereditary instability of thermoresistance in amoebae.

Amoeba↗
PubMed1978

[Quantitative description of the process of cellular radiation inactivation. IX. Remarks on the relative biological effectiveness of ionizing radiations in the reproductive death of diploid and polyploid cells].

The relative biological effectiveness (RBE) has been considered for three kinds of cell radiation damages: subdamages (sublethals), one-track, and two-track lethal damages. In contrast to the "dual theory", which postulates the square relation between the lethal damage yield and the specific energy, it is assumed that the one-track lethal yield is linearly related to the specific energy per cell nucleus. As a result, the identical dependence has been obtained of both one-track lethals and subdamages on specific energy and absorbed dose. It is established that RBE for all three kinds of damages does not depend on the radiation dose. It is shown that RBE for subdamages and one-track lethals depends on LET of radiation only, and involves molecular parameters of sensitive cell structures. Within the limits of this assumption, the relations are general for all the types of eukaryotic cells. These can be used for a further development of the RBE theory, with spectra of LET, the track structure of charged particles, the contribution of delta-electrons etc being taken into consideration.

Cell Division↗
PubMed2004

[Analysis of genetic variation in rare endemic species Oxytropis chankaensis Jurtz. (Fabaceae) using RAPD markers].

The method of polymerase chain reaction with random primers (RAPD) was used to assess genetic variation and population differentiation in the rare endemic plant Oxytropis chankaensis Jurtz. (Fabaceae). DNA samples from plants of two isolated populations were compared at 133 loci detected by use of ten primers. Both populations examined were characterized by high polymorphism levels (P95 = 72.9%, A = 1.92 and P95 = 74.4%, A = 1.88, respectively). They were also statistically significantly different in the frequencies of most of the amplicons. For each of the plants, unique multilocus RAPD phenotype was established using 17 to 20 RAPD markers. Diagnostic markers were not revealed. The populations were poorly differentiated. On average, the between-population component accounted for about 8% of the variation, while 92% of the variation was detected within populations. High variation along with the low degree of differentiation characteristic of two most geographically remote populations of O. chankaensis can have several explanations, among which a polyploid origin of the species seems to be most important.

DNA Primers↗
PubMed1994

Growth and differentiation of the human megakaryoblastic cell line (ELF-153): a model for early stages of megakaryocytopoiesis.

ELF-153 is a cell line that has been established from a patient with a poorly differentiated acute myeloid leukemia associated with an acute myelofibrosis. A majority of cells had a blast morphology with the phenotype of a myeloid hematopoietic progenitor, ie, CD34+, CD33+, CD13+, HLA-DR+, but CD38-, and the remaining cells (5% to 10%) expressed platelet restricted proteins such as CD41, CD42, CD36, CD61, and von Willebrand factor; some of them were polyploid (up to 32N) and exhibited demarcation membranes and alpha granules. No erythroid or other lineage-specific markers were detected. Proliferation of ELF-153 cells was highly stimulated by interleukin-3 (IL-3) and granulocyte-macrophage colony-stimulating factor and to a lesser extent by stem cell factor and IL-6. In contrast, the cell line did not respond to erythropoietin, leukemia inhibitory factor, IL-7, IL-11, granulocyte colony-stimulating factor, and basic fibroblast growth factor. ELF-153 cells could be separated by flow cytometry into three discrete cell populations (CD34+/CD61-, CD34+/CD61+, and CD34-/CD61+) with different proliferative and endomitotic properties corresponding to distinct stages of the mega karyocyte (MK) differentiation. This MK differentiation, which involved a minority of ELF-153, could be increased in the presence of 5-azacytidine and phorbol ester, but could not be significantly modified by growth factors. By contrast, cytochalasin B dramatically induced polyploidization without differentiation. It is noteworthy that association of 5-azacytidine to cytochalasin B dramatically induced the production of polyploid MK cells. To understand the molecular mechanisms underlying this MK differentiation, the expression of GATA-1 and GATA-2 was investigated in subpopulations of ELF-153. A high level of GATA-1 and GATA-2 mRNA was only present in the CD61+ cells. Therefore, these two transactivating factors may play an important role in the MK differentiation of ELF-153. We conclude that ELF-153 might be an important tool to investigate the mechanisms by which transcription factors control differentiation of MK progenitors.

Acute Disease↗
PubMed1999

Differentiation-related changes in the cell cycle traverse.

This review examines recent developments relating to the interface between cell proliferation and differentiation. It is suggested that the mechanism responsible for this transition is more akin to a "dimmer" than to a "switch," that it is more useful to refer to early and late stages of differentiation rather than to "terminal" differentiation, and examples of the reversibility of differentiation are provided. An outline of the established paradigm of cell cycle regulation is followed by summaries of recent studies that suggest that this paradigm is overly simplified and should be interpreted in the context of different cell types. The role of inhibitors of cyclin-dependent kinases in differentiation is discussed, but the data are still inconclusive. An increasing interest in the changes in G2/M transition during differentiation is illustrated by examples of polyploidization during differentiation, such as megakaryocyte maturation. Although the retinoblastoma protein is currently maintaining its prominent role in control of proliferation and differentiation, it is anticipated that equally important regulators will be discovered and provide an explanation at the molecular level for the gradual transition from proliferation to differentiation.

Animals↗
PubMed2026

Cultivar-dependent regulation of cytokinin biosynthesis in wheat: developmental expression of TaIPT genes and hormonal crosstalk during reproductive development.

BACKGROUND: Cytokinins are key regulators of plant growth, reproductive development, and yield formation. In cereals, cytokinin biosynthesis is catalyzed by isopentenyltransferase (IPT) enzymes, yet the genomic organization and developmental regulation of IPT genes in polyploid wheat remain incompletely understood, especially at the cultivar level. RESULTS: Here, we present an integrated genomic, transcriptional, and hormonal analysis of the TaIPT gene family during vegetative and reproductive development in two wheat cultivars, awnless Kontesa and awned Ostka. Genome-wide analysis identified nine core TaIPT genes represented by 25 homoeologs distributed across the A, B, and D subgenomes, for which a unified nomenclature was established. Phylogenetic analysis resolved TaIPTs into conserved evolutionary clades corresponding to ATP/ADP-dependent and tRNA-dependent IPT groups. Expression profiling revealed distinct spatial and temporal patterns of TaIPT transcription across roots, leaves, inflorescences, and developing spikes. Several TaIPT genes showed enhanced expression during early reproductive stages, coinciding with dynamic changes in cytokinin concentrations. Comparative analyses revealed cultivar-specific expression and co-variation patterns, with Kontesa displaying more compartmentalized TaIPT expression and Ostka showing coordinated activation of multiple TaIPT genes during early grain development. Hormone profiling further indicated stage-dependent associations between TaIPT expression, cytokinin metabolism, and the balance between cytokinins and abscisic acid. These relationships are interpreted as correlative and provide a framework for future functional testing rather than direct evidence of causality. CONCLUSIONS: Together, these results provide a cultivar-focused framework for understanding the organization and regulation of cytokinin biosynthesis genes in wheat. The data highlight cultivar-dependent TaIPT expression patterns and their association with cytokinin dynamics during reproductive development, while also identifying the need for homoeolog-specific and functional validation. This study establishes a foundation for future research on cytokinin-mediated regulation of wheat growth and grain development.

Triticum↗
PubMed1981

Smooth muscle cell hypertrophy versus hyperplasia in hypertension.

Arteries of hypertensive animals have a greater mass of smooth muscle than those of normotensive controls. We examined the contribution of smooth muscle cell hypertrophy and hyperplasia to this increase in mass. Cell size measurements obtained by (i) image analysis of enzyme-dispersed cells, (ii) morphometric evaluation of tissue sections, and (iii) biochemical measures of protein/cell and actin/cell ratios on isolated cells showed that average cell size was greater in spontaneously hypertensive rats than in normotensive Wistar-Kyoto and Sprague-Dawley controls. Average DNA/cell ratios were also increased in spontaneously hypertensive rats while protein/DNA ratios were not different. Analysis of nuclear DNA content of individual cells by flow microfluorimetry and Feulgen-DNA microdensitometry measurements showed that greater than 20% of spontaneously hypertensive rats cells were polyploid while less than 10% of control cells were polyploid. Estimates of cell number per centimeter of aortic length, based on ploidy and DNA content, show no difference between control and hypertensive rats. Thus, smooth muscle hypertrophy alone accounts for the increased mass of smooth muscle in aortas of spontaneously hypertensive rats. Furthermore, this cellular hypertrophy is accompanied by a change in nuclear ploidy. This nuclear response in hypertension may represent a fixed change related to the establishment of a chronic hypertensive state.

Actins↗
PubMed2005

Caspases-dependent cleavage of mitotic checkpoint proteins in response to microtubule inhibitor.

The mitotic checkpoint ensures the fidelity of chromosomal segregation by delaying the onset of anaphase until all chromosomes are aligned on the metaphase plate. After sustained mitotic arrest, however, cells eventually exit mitosis without the mitotic checkpoint being silenced. These cells then undergo apoptosis, an event that is important for prevention of the chromosomal instability observed in human cancers. An interesting question is to establish the biochemical link between the mitotic checkpoint and the subsequent apoptotic cell death. Here, we found that following prolonged spindle damage, the mitotic checkpoint kinases such as Bub1 and BubR1 were cleaved through a mechanism sensitive to caspases inhibitor. Interestingly, the expression of these mutants resistant to caspases-dependent cleavage led to increased apoptosis after sustained mitotic arrest, and a correspondingly more efficient elimination of the polyploid population than that seen in cells expressing wild-type proteins. These findings provide the novel biochemical properties of mitotic checkpoint proteins through its cleavage by caspases-dependent manner.

Apoptosis↗
PubMed2001

Characterisation of epithelial cell line from rat cornea.

PURPOSE: Characterisation of RtCE-1 cells, newly established rat corneal epithelial cell line. METHODS: Morphology of RtCE-1 cells was characterised by light and electron microscopy. Expression of cytokeratins was studied by polyacrylamide electrophoresis and Western blotting. Characterisation of RtCE-1 cells also included karyotype analysis and in vitro study of growth kinetics. RESULTS: The line shows morphological similarities to normal corneal epithelium. The cells express cornea-specific cytokeratins. Karyotype analysis revealed that the cells are polyploid with modal number of chromosomes at passage 30 equalling 72 +/- 14. Growth of the line is partially dependent on EGF. CONCLUSION: RtCE-1 cells may constitute a model for the evaluation of proliferation, function and differentiation of corneal epithelium in vitro.

Animals↗
PubMed2000

Characterization of the biological and biochemical activities of F 11782 and the bisdioxopiperazines, ICRF-187 and ICRF-193, two types of topoisomerase II catalytic inhibitors with distinctive mechanisms of action.

F 11782 is a newly identified catalytic inhibitor of topoisomerases I and II, without any detectable interaction with DNA. This study aimed to establish whether its catalytic inhibition of topoisomerase II was mediated by mechanisms similar to those identified for the bisdioxopiperazines. In vitro combinations of F 11782 with etoposide resulted in greater than additive cytotoxicity in L1210 cells, contrasting with marked antagonism for combinations of etoposide with either ICRF-187 or ICRF-193. All three compounds caused a G2/M blockade of P388 cells after an 18-h incubation, but by 40 h polyploidization was evident only with the bisdioxopiperazines. Gel retardation data revealed that only F 11782, and not the bisdioxopiperazines, was capable of completely inhibiting the DNA-binding activity of topoisomerase II, confirming its novel mechanism of action. Furthermore, unlike ICRF-187 and ICRF-193, the cytotoxicity of F 11782 appeared mediated, at least partially, by DNA damage induction in cultured GCT27 human teratoma cells, as judged by a fluorescence-enhancement assay and monitoring p53 activation. Finally, the major in vivo antitumor activity of F 11782 against the murine P388 leukemia (i.v. implanted) and the B16 melanoma (s.c. grafted) contrasted with the bisdioxopiperazines' general lack of activity. Overall, F 11782 and the bisdioxopiperazines appear to function as quite distinctive catalytic topoisomerase II inhibitors.

Animals↗
PubMed2004

[Antiproliferative effect of bcl-2 gene does not concern the control of mitotic events].

E1A + c-Ha-ras-transformants overexpressing bcl-2 oncogene are able to be arrested at the G1/S boundary of the cell cycle after DNA damage and upon serum starvation, this cell cycle blockage being accompanied by a decrease in the activity of cyclin E--Cdk2 complexes. Roscovitine-induced inhibition of cyclin-dependent kinases (Cdks) activity does not result in the G1/S arrest of E1A + c-Ha-ras + bcl-2-transformants. Roscovitine treatment causes an accumulation of G2/M cells, mainly at the expense of mitotic cells. However, the expression of Bcl-2 oncoproducts does not re-establish the regulation of mitotic events broken by introduction of E1A and c-Ha-ras oncogenes in normal cells, as revealed by the treatment of E1A + c-Ha-ras + bcl-2-transformants with nocodazole inducing mitotic arrest in normal cells. In spite of the elevated expression of antiapoptotic bcl-2 gene in transformants, nocodazole treatment results in mass apoptotic death preceded by polyploidy. Roscovitine also induces apoptosis with no polyploid cell accumulation being observed. Inhibition of Cdks activity with Roscovitine, as well as violation of microtubule depolymerization with nocodazole result in the apoptotic death in the tested cell lines sensitive (E1A + c-Ha-ras) and resistant (E1A + c-Ha-ras + bcl-2) to damaging agents. Thus, the application of Roscovitine, a specific inhibitor of Cdks, suggests that the decrease in Cdks activity in E1A + c-Ha-ras + bcl-2-transformants is not likely to be responsible for G1/S cell cycle arrest realization after damaging influences. Moreover, an antiproliferative effect of Bcl-2 in E1A + c-Ha-ras-transformants is restricted by restoration of cell cycle events at G1/S and G2/M boundaries, and does not concern the program of mitotic events regulation.

Adenovirus E1A Proteins↗
PubMed1988

Vascular smooth muscle polyploidy in the development and regression of hypertension.

1. Two groups of spontaneously hypertensive rats (SHR) were treated with enalapril (25-30 mg/kg per day): Group I received treatment from 4 to 14 weeks of age to inhibit development of hypertension and Group R received the drug from 14 to 20 weeks of age to reverse established hypertension. 2. Systolic blood pressure, ploidy of aortic smooth muscle cells (flow cytometric DNA analysis) and aortic hypertrophy (medial cross-sectional area) were determined at times both during and after enalapril treatment (up to 30 weeks). 3. Enalapril treatment normalized blood pressure to that of age-matched Wistar-Kyoto rats in both groups. Blood pressure rose again following cessation of treatment. 4. In untreated SHR the incidence of polyploid cells increased concomitantly with increasing pressure throughout the time studied, whereas in Group I the incidence remained low. In Group R, the incidence of polyploidy directly paralleled both the decrease (normalization) and the rise in blood pressure following cessation of treatment. 5. Hence, the incidence of vascular smooth muscle cell polyploidy is not simply a result of growth of the vessel with increasing age of the SHR, but parallels inhibition, reversal, and redevelopment of hypertension.

Aging↗
PubMed1983

Establishment and characterization of a human non-secretory plasmacytoid cell line and its hybridization with human B cells.

A human non-secretory plasmacytoid cell line has been established for 6 years in more than 170 passages. Over 300 passages have been made from several early and late passages. The cell line is karyotypically normal, easily grown and has the characteristic features of a non-secretory plasmablast. Its characteristics suggest its use for hybridization by new methods as well as a study of its secretory defect. HPRT-negative phenotypic mutants can be derived from this line and a single polyploid clone has also been isolated. Hybridization with the HPRT+ and HPRT- lines X human B cells is described.

Aged↗
PubMed1997

Uncoupling of S-phase and mitosis by recombinant cytotoxic necrotizing factor 2 (CNF2).

Cytotoxic necrotizing factor 2 (CNF2) is an exotoxin identified from virulent clinical isolates of Escherichia coli. It has been characterized in adherent cell lines as an inducer of cellular death, hyperploidy (multinucleation), and cytoskeletal reorganization. The molecular mechanism of these actions is unclear. Two cellular mechanisms can be hypothesized to explain the DNA content increase (hyperploidy) induced by the toxin. The first is that the toxin interferes with cytoplasmic division without interfering with normal nuclear cycling, such that DNA is replicated in the absence of cell division. The second is that the toxin drives the nuclear machinery to replicate the DNA multiple times within one cell cycle, without interfering with cytoplasmic division. In order to investigate these phenomena, we have constructed a recombinant CNF2 gene that expresses a toxin with both an epitope tag and a polyhistidine tag. Extracts made from E. coli that express this gene have a high multinucleating activity that colocalizes with the recombinant 115-kDa protein. To distinguish between these hypotheses, we used recombinant CNF2 and several growth conditions (time, partial differentiation, and stage of growth) to establish a relationship between cellular divisions and generation of hyperploidy. It was also determined that the toxin had no effect upon in vitro DNA replication using a Xenopus egg extract system. In aggregate, these data are consistent with the hypothesis that CNF2 is affecting cytoplasmic division and thereby removing the requirement for a completed mitosis before the initiation of another S-phase. These data are discussed in relation to the generation of polyploid cells during megakaryopoeisis and the generation of aneuploid cells during tumorigenesis.

3T3 Cells↗
PubMed2002

Regulation of CDC6, geminin, and CDT1 in human cells that undergo polyploidization.

Endomitosis is the process by which mammalian megakaryocytes become polyploid during terminal differentiation. As in other endoreplicating cells, cyclin-cdk complexes are distinctly regulated, probably to overcome the strict mechanisms that prevent rereplication in most somatic cells. We have asked whether key factors involved in the assembly and licensing of replication origins are equally regulated during endomitosis. Cdc6, cdt1, and geminin expression was analyzed during differentiation of two human megakaryoblastic cell lines, HEL and K562, which respectively do and do not establish endoreplication cycles. Geminin was downregulated, whereas cdt1 levels were maintained upon differentiation of both cell lines, independently of whether cells entered extra S-phases. In contrast, cdc6 was present and remained nuclear only in differentiated endoreplicating cells. Interestingly, cdc6 protein expression was reestablished in K562 cells that underwent endomitosis after transient or stable cyclin E overexpression. The high levels of cyclin E reached in these cells appeared to influence the stabilization of cdc6 protein rather than its RNA transcription rate. Finally, cdc6 overexpression drove HEL cells into endoreplication cycles in the absence of differentiation stimuli. Our results show that both cdt1 and cdc6 are differentially regulated during megakaryocytic differentiation and suggest an active role of cdc6 in endomitosis.

Cell Cycle↗
PubMed2026

Complete telomere-to-telomere genome assembly of Guazuma ulmifolia uncovers evolutionary mechanisms, drought adaptation, and flavonoid biosynthesis.

The first T2T reference genome of Guazuma ulmifolia is reported, which serves as a core genomic resource for stress adaptation research and stress-tolerant breeding in cacao wild relatives. Climate change, particularly increased incidence of drought, poses a major threat to food security. Understanding the genomic basis of environmental adaptation in crop wild relatives can provide valuable resources for improving stress resilience. Guazuma ulmifolia, a wild relative of Theobroma cacao with important ecological and medicinal value, lacks high-quality reference genomic resources. Here, we report the first telomere-to-telomere (T2T) chromosome-level genome assembly of G. ulmifolia, with a genome size of 311.31 Mb, contig N50 of 35.19 Mb, and 98.70% BUSCO completeness. Repetitive sequences constitute 27.43% of the G. ulmifolia genome, with LTR retrotransposons as the predominant class. Comparative genomic analyses revealed that genome-size variation among Malvaceae species is associated with differences in polyploidization history and TE dynamics. Ancestral karyotype reconstruction identified five lineage-specific chromosome fusion events distinguishing G. ulmifolia from T. cacao. Comparative analyses further identified tandem duplication-associated expansion of stress-related LEA and GST gene families, suggesting potential genomic features associated with stress responses. Flavonoid biosynthesis genes were largely conserved in copy number but showed tissue-specific expression patterns, providing candidate genes for investigating secondary metabolism. Together, this study establishes a high-quality T2T genome resource for exploring genome evolution, chromosome organization, and stress-related genomic features in Malvaceae.

Genome, Plant↗
PubMed2003

Evolutionary dynamics of duplicated genes in plants.

Gene duplication, arising from region-specific duplication or genome-wide polyploidization, is a prominent feature in plant genome evolution. Understanding the mechanisms generating duplicate gene copies and the subsequent dynamics among gene duplicates is vital because these investigations shed light on regional and genome-wide aspects of evolutionary forces shaping intra- and interspecific genome contents, evolutionary relationships, and interactions. This review discusses recent gene duplication analyses in plants, focusing on the molecular and evolutionary dynamics occurring at three different timescales following duplication: (1). initial establishment and persistence of cytotypes, (2). interactions among duplicate gene copies, and (3). longer term differentiation between duplicated genes. These relative time points are presented in terms of their potential adaptive significance and impact on plant evolutionary genomics research.

Adaptation, Biological↗
PubMed2005

Structural and numerical chromosome changes in colon cancer develop through telomere-mediated anaphase bridges, not through mitotic multipolarity.

Telomere dysfunction has been associated with chromosomal instability in colorectal carcinoma, but the consequences of telomere-dependent instability for chromosome integrity and clonal evolution have been little explored. We show here that abnormally short telomeres lead to a wide spectrum of mitotic disturbances in colorectal cancer cell lines, including anaphase bridging, whole-chromosome lagging, and mitotic multipolarity. These abnormalities were found in both the presence and absence of microsatellite instability. The mean telomere length varied extensively between cells from the same tumor, allowing the establishment of tumor cell subpopulations with highly different frequencies of mitotic disturbances. Anaphase bridging typically resulted in either inter-centromeric chromatin fragmentation or centromere detachment, leading to pericentromeric chromosome rearrangements and loss of whole chromosomes, respectively. There was a strong correlation between anaphase bridges and multipolar mitoses, and the induction of dicentric chromosomes by gamma irradiation and telomerase inhibition led to an elevated frequency of multipolar mitotic spindles, suggesting that multipolarity could result from polyploidization triggered by anaphase bridging. Chromatid segregation in multipolar mitoses was close to random, resulting in frequent nullisomies and nonviable daughter cells. In contrast, there was a high clonogenic survival among cells having gone through anaphase bridging in bipolar mitoses. Bridging of telomere-deficient chromosomes could thus be a major mutational mechanism in colorectal cancer, whereas mitotic multipolarity appears to be a secondary phenomenon that rarely, if ever, contributes to clonal evolution.

Anaphase↗