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Results for “polyploidization”

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PubMed1996

On the theory of partially inbreeding finite populations. IV. The effective population size for polyploids reproducing by partial selfing.

Consider a population of size N in which there is reproduction by selfing with probability beta and by random mating with probability 1-beta. In each cell of any individual, homologous chromosomes appear 2n times, with n among them having been contributed by each parent. Wright [Proc. Natl. Acad. Sci. 24:372 (1938)] showed that if beta = 0, there is no double reduction in gamete formation, and a Poisson offspring distribution, the probability of nonidentity by descent of two random copies of a gene in an individual of generation t + 1 is approximately 1-1/2nN times as large as it is in generation t if N is large. This result will be generalized to populations with any beta > or = 0 and any offspring distribution. If n = 2 or 3, a result will be obtained that also holds for any probability of double reduction.

Inbreeding↗
PubMed1990

High levels of chromosome instability in polyploids of Saccharomyces cerevisiae.

The yeast Saccharomyces cerevisiae was used to study the genetic consequences of polyploidy in a unicellular organism. Isogenic diploid (2N), triploid (3N) and tetraploid (4N) strains with a genetically marked chromosome VII (cyh2-leu1-CEN7-ade6) were constructed and were used to follow the loss of one, two or three chromosome VII's during mitosis. We found that as ploidy increased, the frequency of loss of a single chromosome VII increased: Loss of one copy of chromosome VII occurred at a rate nearly 30-fold higher in triploids and approximately 1000-fold higher in tetraploids than in the diploid. Loss of two or three copies occurred at an even greater frequency. These findings suggest either that aneuploidy (3N-1, 3N-2, 4N-1, 4N-2, 4N-3) increases genome instability or that multiple chromosome loss events occur at high frequency. Polyploidy appears to dramatically increase chromosome loss, presumably due to the inability of the cell to undergo proper chromosome segregation. The biological significance and possible causes for the instability of polyploidy in unicellular organisms such as yeast are discussed.

Chromosomes, Fungal↗
PubMed1987

Establishment and characterization of a polyploid mouse myeloid leukemia cell line useful for in-vivo examination of cell proliferation kinetics.

A near-tetraploid cell line (LL-1) was established from mouse myeloid leukemia Ml cells. This paper reports characterization of the LL-1 cells and the in-vivo detection of the leukemia cells transplanted in syngeneic mice. The LL-1 cells are myeloblastic and grow well in suspension culture. Morphological analysis showed that the nucleus of LL-1 cells was almost twice as large as that of the parent line cells. The modal chromosome number of LL-1 cells was 75, and the DNA index determined by flow cytometry was 2.3. The cells were unresponsive to the inducer of differentiation of M1 cells. Transplantation experiments showed that the LL-1 cells were leukemogenic in syngeneic SL mice: ten mice inoculated i.p. with LL-1 cells (4 X 10(6)) all died of leukemia within 6 weeks. The cells in the peritoneal cavity were collected at appropriate times during progression of the leukemia. On microscopic examination the LL-1 cells were clearly distinguishable from normal host cells in the peritoneal cavity by the size of their nucleus. Counts showed that their number decreased markedly during the first 2 weeks after their transplantation, and then increased about ten times in a week. By 4 or 5 weeks after transplantation these LL-1 cells filled the peritoneal cavity. These large-sized leukemia cells that grow in syngeneic mice will be useful for investigating the mechanisms of in-vivo responses of leukemia cells to various therapeutic treatments.

Animals↗
PubMed1987

Increased tumorigenicity of polyploid Ehrlich variants during growth in vivo is associated with karyotypic changes.

In previous studies, treatment of Ehrlich ascites tumors (EAT) with either Sendai virus, Herpes virus or neuraminidase produced variants that differed significantly from EAT in both tumorigenicity and karyotype. In this study, less tumorigenicity variants of EAT were isolated by culturing in media containing low concentrations of serum or without serum. In contrast to the relative stability of tumorigenicity in such variants cultured in vivo, the tumorigenicity of these variant clones passaged in vivo was variable, depending on the variant clone. During growth in vivo, 3 variant clones independently isolated from serum-free medium, low serum-containing medium and after neuraminidase treatment produced markedly heterogeneous tumors, and after 4 passages the tumors were about 1000 times more tumorigenic than the initial variants. In generating new tumors, the tumors always segregated chromosomes. The banded chromosome analysis of a variant clone isolated from serum-free medium and its malignant tumor showed that most of the chromosomes segregated from the clone were normal types. On the other hand, the tumorigenicity of Herpes virus-induced variants was unchanged during growth in vivo.

Animals↗
PubMed1985

Growth and polyploidization of the liver of early postnatal rats treated with bleomycin.

Bleomycin was administered to 6- and 10-day-old rats and its effects were examined after a two-week survival period. Decreases in body weight and some phenotype abnormalities occurred in both age groups. Decreased relative liver weight (g/g b.w.) was observed only in animals injected on PD 10. DNA microdensitometry and microfluorometry (Feulgen reaction and Hoechst 33342 staining) revealed an increase in the frequency of intermediate DNA values in animals injected on PD6 and killed on PD20. In older animals, i.e. in rats injected on PD10 and killed on PD25, increases in 4c mononucleate and 8c binucleate cells and also a reduction of the relative number of binucleate cells appeared, as compared with age-matched controls. In both age groups, karyological abnormalities, including micronucleate cells and imbalanced DNA content in binucleate cells, were observed.

Aging↗
PubMed2005

Endomitosis and polyploidization of myocardial cells in the periphery of human acute myocardial infarction.

OBJECTIVE: Although the genetic program for reinitiating DNA synthesis exists in post-mitotic cardiomyocytes, and it was reported that in human acute myocardial infarction (AMI) a significant proportion of myocytes enter mitosis, the rule is that the lost tissue is replaced by a collagen scar. The purpose of this study was to search for the basis of this discordance in order to devise future strategies to induce division of myocytes into daughter cells that may replace the lost tissue with contractile cells. METHODS: In 15 human hearts with 1- to 21-day-old infarcts, the expression of the cell cycle proteins Ki67 antigen, cyclins D, A, and B1, the presence of mitotic bodies, and the ploidy status were investigated with immunoenzymatic methods, light and laser confocal microscopy, and densitometry in the myocytes surrounding the infarct area. RESULTS: In 7- to 13-day-old infarcts, 11.61+/-6.94% of the myocytes presented Ki67+ nuclei, and a lower proportion presented cyclins D, A, and B. At earlier and later times, the proportion of Ki67+ myocytes was significantly lower. Although under confocal microscopy and fluorescent labels, some of the Ki67+ myocytes appeared to be in different stages of mitosis, with Nomarski optics and hematoxylin counterstaining, the condensed chromosomes, although arranged in metaphase and anaphase plates or split in sister chromatids, were always located within a preserved nuclear envelope, indicating the presence of endomitosis. Conventional mitosis was exceptionally observed. In the 14- and 21-day-old infarcts, the ploidy of the myocytes adjacent to the infarct was significantly higher than in distant zones. CONCLUSION: These observations indicate that in human infarcts, entrance of cardiomyocytes into the cell cycle is transient and that endomitosis, leading to polyploidy, rather than mitosis, leading to karyokinesis, is the final fate of cycling cells. Both observations may account for the discordance between the regenerative ability of myocytes and the lack of an efficient reparative process in human AMI.

Adult↗
PubMed2005

Segregation of genomes in polyploid tumour cells following mitotic catastrophe.

Following irradiation p53-function-deficient tumour cells undergo mitotic catastrophe and form endopolyploid cells. A small proportion of these segregates nuclei, and give rise to viable descendants. Here we studied this process in five tumour cell lines. After mitotic failure, tumour cells enter the endocycle and form mono-nucleated or multi-nucleated giant cells (MOGC and MNGC). MNGC arise from arrested anaphases, MOGC, from arrested metaphases. In both cases the individual genomes establish a radial pattern by links to a single microtubule organizing centre. Segregation of genomes is also ordered. MNGC present features of mitosis being resumed from late anaphase. In MOGC the sub-nuclei retain arrangement of stacked metaphase plates and are separated by folds of the nuclear envelope. Mitosis then resumes in sub-nuclei directly from metaphase. The data presented indicate that endopolyploid tumour cells preserve the integrity of individual genomes and can potentially re-initiate mitosis from the point at which it was interrupted.

Cell Line, Tumor↗
PubMed2006

Polyploid hybrids: multiple origins of a treefrog species.

Hyla versicolor, a tetraploid treefrog, is reported to have originated via multiple hybridization events involving three diploid ancestors. Its complex reticulate history provides insights into the roles that polyploidy and hybridization can play in the origin of species.

Animals↗
PubMed2005

Hid can induce, but is not required for autophagy in polyploid larval Drosophila tissues.

The major cell death pathways are apoptosis and autophagy-type cell death in Drosophila. Overexpression of proapoptotic genes in developing imaginal tissues leads to the activation of caspases and apoptosis, but most of them show no effect on the polytenic cells of the fat body during the last larval stage. Surprisingly, overexpression of Hid induces caspase-independent autophagy in the fat body, as well as in most other larval tissues tested. Hid mutation results in inhibition of salivary gland cell death, but the disintegration of the larval midgut is not affected. Electron microscopy shows that autophagy is normally induced in fat body, midgut and salivary gland cells of homozygous mutant larvae, suggesting that Hid is not required for autophagy itself. Constitutive expression of the caspase inhibitor p35 produces identical phenotypes. Our results show that the large, post-mitotic larval cells do not react or activate autophagy in response to the same strong apoptotic stimuli that trigger apoptosis in small, mitotically active imaginal disc cells.

Animals↗
PubMed2004

Polyploid and multilocus extensions of the Wahlund inequality.

Wahlund's inequality informally states that if a structured and an unstructured population have the same allele frequencies at a locus, the structured population contains more homozygotes. We show that this inequality holds generally for ploidy level P, that is, the structured population has more P-polyhomozygotes. Further, for M randomly chosen loci (M >or= 2), the structured population is also expected to contain more M-multihomozygotes than an unstructured population with the same single-locus homozygosities. The extended inequalities suggest multilocus identity coefficients analogous to F(ST). Using microsatellite genotypes from human populations, we demonstrate that the multilocus Wahlund inequality can explain a positive bias in "identity-in-state excess".

Chromosome Mapping↗