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PubMed2003

Breaking down taxonomic barriers in polyploidy research.

Polyploidy is important in the evolutionary history of plants, and it has played a crucial role in shaping the genome structures of all eukaryotes. New and rapidly improving techniques in genomics, cytogenetics and molecular ecology have resulted in a dramatic increase in publications about duplicate genes, genome rearrangements and detection of ancient duplication events. Similarly, research associated with the origins of polyploidy, its persistence in natural populations and the resulting ecological consequences is receiving more attention. Although polyploidy research has been conducted using both animal and plant systems, inferences based on cross-disciplinary comparisons have been rare. Here, I review recent developments in the field in both plants and animals, emphasizing the benefits of communication between the two groups.

Animals↗
PubMed1986

Flow cytometry of renal oncocytoma: common occurrence of deoxyribonucleic acid polyploidy and aneuploidy.

Flow cytometry was performed on 51 typical specimens of renal oncocytoma. Nuclei were extracted from paraffin-embedded archival material and isolated nuclei were stained with propidium iodide. Of the 51 available tissue blocks 86 per cent were evaluable and 50 per cent of these samples showed a deoxyribonucleic acid (DNA) histogram that was approximately the same as normal renal parenchyma. Of the oncocytoma samples 39 per cent showed a marked increase (more than 10 per cent of the nuclei) in the tetraploid DNA peak, while 11 per cent showed a distinct DNA aneuploid peak. Among 21 evaluable grade 2 oncocytic renal tumors 33 per cent showed a normal DNA histogram, 43 per cent showed a marked increase in the DNA tetraploid peak and 24 per cent showed a DNA aneuploid peak. The common presence of polyploid nuclei containing double quantities of chromosomal DNA may correlate with the long-standing pathological observation that oncocytic tumors often contain a distinct population of large nuclei. Indeed, 86 per cent concurrence was seen between the detection of an abnormal DNA content by flow cytometry and the histopathological presence of large abnormal nuclei in these specimens. Since renal oncocytomas (grade 1 oncocytic tumors) rarely, if ever, metastasize and are relatively noninvasive locally, their markedly abnormal flow cytometry patterns are of considerable interest. Moreover, DNA polyploidy has not been identified previously in renal tumors. The biological significance and mechanism of DNA polyploidy, and the relationship of DNA polyploidy and DNA aneuploidy to the pathogenesis of oncocytic renal tumors require further laboratory investigation. The clinical use of flow cytometry to classify and to predict the behavior of renal tumors will be complicated, since renal oncocytomas commonly have polyploid and aneuploid DNA histograms.

Adenoma↗
PubMed1999

Chromosomal aberrations in transitional cell carcinoma that are predictive of disease outcome are independent of polyploidy.

OBJECTIVE: To determine whether aneusomy for chromosomes 7, 9 and 17 (reported to predict recurrence in up to 65% of patients with superficial transitional cell bladder cancer and thus providing the opportunity for early and effective treatment) reflects specific genetic events on these chromosomes or merely wider unspecific genetic damage to the cell, e.g. that increased copy numbers for 7 and 17 reflect tumour polyploidy. MATERIALS AND METHODS: The study comprised 25 primary tumours; 6 microm thick sections from formalin-fixed and paraffin-embedded tumours were analysed. Chromosome copy numbers were determined by fluorescence in situ hybridization (FISH) using pericentromeric probes for chromosomes 7, 8, 9, 10, 11 and 17. A minimum of 200 nuclei per tumour area were scored by two independent observers. RESULTS: Eight of the 25 tumours examined (32%) showed no evidence of chromosomal abnormalities as detected by FISH for any chromosomes analysed. Twelve tumours (48%) showed abnormalities for one or two chromosomes, five tumours (20%) showed abnormalities for multiple chromosomes and one tumour showed abnormalities for all chromosomes analysed, suggestive of polyploidy. CONCLUSIONS: Chromosomal abnormalities predictive of recurrence occur largely in the absence of other gross chromosomal lesions. In a small proportion of cases other chromosomes are affected, but this is almost always distinct from tumour polyploidy.

Carcinoma, Transitional Cell↗
PubMed1999

Noscapine hydrochloride disrupts the mitotic spindle in mammalian cells and induces aneuploidy as well as polyploidy in cultured human lymphocytes.

Noscapine hydrochloride is a centrally acting antitussive opium derivative widely used in cough suppressants. Recent studies have reported that noscapine is a potent inducer of polyploidy but not of aneuploidy in vitro. To obtain more comprehensive information about the cytogenetic effects of this compound, we treated cultured human lymphocytes (HPL) and Chinese hamster ovary (CHO) cells with various concentrations of noscapine hydrochloride. Using a differential staining technique noscapine was shown to disrupt the mitotic spindle at concentrations < 5 micrograms/ml in both cell types. The use of multicolor fluorescence in situ hybridization (FISH) on noscapine-treated human lymphocytes showed a dose-dependent induction of hyperdiploidy of chromosome 1 but not of chromosomal breakage in the 1cen-q12 region under in vitro conditions, indicating that noscapine is specifically inducing numerical chromosomal aberrations. FISH with probes targeting different chromosomes revealed that noscapine is capable of inducing both polyploidy and true hyperdiploidy. Our results show that noscapine, by disrupting the function of the mitotic spindle, has the ability to induce aneuploidy and not uniquely polyploidy as previously reported. By using these types of molecular cytogenetic techniques, it should be possible to evaluate the ability of noscapine to induce aneuploidy in the upper intestinal tract in vivo.

Aneuploidy↗
PubMed1989

Effect of enalapril on aortic smooth muscle cell polyploidy in the spontaneously hypertensive rat.

The angiotensin converting enzyme (ACE) inhibitor enalapril was used to examine the effects of inhibition, regression and redevelopment of hypertension on the ploidy of aortic smooth muscle cells in spontaneously hypertensive rats (SHR). The incidence of polyploidy cells, as determined by flow cytometric DNA analysis, directly paralleled changes in systolic blood pressure. When the development of hypertension was inhibited by treatment with enalapril, the incidence of polyploid cells remained low compared with untreated age-matched SHR. Likewise, when the blood pressure of hypertensive animals was lowered by enalapril treatment, the incidence of polyploid cells decreased. Addition of enalapril to primary cultures of smooth muscle had no direct effect on proliferation or the incidence of polyploidy. These results suggest that angiotensin II may be involved in the development of vascular smooth muscle polyploidy in vivo, either by a direct effect on the cells or indirectly by elevating blood pressure or by potentiation of sympathetic discharge.

Angiotensin II↗
PubMed2004

Functional divergence of duplicated genes formed by polyploidy during Arabidopsis evolution.

To study the evolutionary effects of polyploidy on plant gene functions, we analyzed functional genomics data for a large number of duplicated gene pairs formed by ancient polyploidy events in Arabidopsis thaliana. Genes retained in duplicate are not distributed evenly among Gene Ontology or Munich Information Center for Protein Sequences functional categories, which indicates a nonrandom process of gene loss. Genes involved in signal transduction and transcription have been preferentially retained, and those involved in DNA repair have been preferentially lost. Although the two members of each gene pair must originally have had identical transcription profiles, less than half of the pairs formed by the most recent polyploidy event still retain significantly correlated profiles. We identified several cases where groups of duplicated gene pairs have diverged in concert, forming two parallel networks, each containing one member of each gene pair. In these cases, the expression of each gene is strongly correlated with the other nonhomologous genes in its network but poorly correlated with its paralog in the other network. We also find that the rate of protein sequence evolution has been significantly asymmetric in >20% of duplicate pairs. Together, these results suggest that functional diversification of the surviving duplicated genes is a major feature of the long-term evolution of polyploids.

Arabidopsis↗
PubMed1994

Polyploidy in non-neoplastic tissues.

AIM: To investigate the prevalence and amount of polyploidy in fine needle aspiration specimens of the liver, urinary cytospin preparations, and cytospin preparations from pleural and peritoneal fluid. METHODS: Cells from 44 liver smears, 48 urine specimens, and 46 pleural and peritoneal aspirations were examined. After Feulgen restaining the DNA content of 100 randomly selected nuclei was determined using a TAS-plus image analysis system, combined with an automated microscope. RESULTS: Polyploidy was observed up to 16c in the liver, and up to 8c in urothelium and mesothelium. Sixty eight per cent of the liver aspirates contained polyploid nuclei. The rate in urothelium was 20.8% and in mesothelium 6.5%. CONCLUSIONS: Polyploidy in the liver may be interpreted as being associated with tissue differentiation, but the findings in urothelium and mesothelium remain of unknown importance.

Aged↗
PubMed1997

Expression of functional beta-adrenoceptors and polyploidy development in cultured vascular smooth muscle cells from spontaneously hypertensive rats.

The main objective of this study was to investigate the role of beta-adrenoceptor activation in the development of polyploidy in these cells. Smooth muscle cells (SMCs) were cultured from 3- to 4-, 10- to 12-, and 28- to 30-week-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Functional expression of beta-adrenoceptors was examined by treatment of cultured SMCs with a nonselective beta-adrenoceptor agonist, isoproterenol, or an adenylate cyclase activator, forskolin, or a membrane-permeable analog of adenosine 3',5'-cyclic monophosphate (cAMP), 8-bromo-cAMP, and the measurement of intracellular cAMP levels, using a radioimmunoassay. The effects of these treatments on polyploidy development were also studied by measuring the DNA content of SMCs, using scanning microdensitometry. Treatments with isoproterenol or forskolin increased intracellular cAMP levels in both strains of rats in all three age groups. Addition of the beta-adrenoceptor antagonist DL-propranolol inhibited the isoproterenol-stimulated response in SMCs from both SHR and WKY in all three age groups. The number of polyploid SMCs was significantly increased by treatments with isoproterenol, forskolin, or 8-bromo-cAMP in SMCs from 3- to 4-week-old WKY and SHR, but in the 10- to 12-week age group, an increase was found only in SMCs from WKY. Such treatments had no effect on the incidence of polyploid SMCs in the 28- to 30-week groups. We conclude that (i) beta-adrenoceptors expressed by the SMCs from WKY and SHR at all three ages are functional and are coupled via Gs proteins to the stimulation of adenylate cyclase, (ii) treatments that elevate intracellular cAMP levels (by activation of beta-adrenoceptors or of adenylate cyclase) lead to increased polyploid SMCs from WKY and SHR in the younger age group, confirming a role for the beta-adrenoceptor-adenylate cyclase pathway in the development of polyploidy in cultured SMCs from both of these strains of rats, and (iii) the absence of these treatment effects in the induction of polyploid SMCs in older age groups suggests that in these cells, other factors or processes may be involved in regulating the development of polyploid SMCs.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1987

Inhibition of nuclear polyploidy by propranolol in aortic smooth muscle cells of hypertensive rats.

The ability of propranolol to inhibit the development of polyploidy in aortic vascular smooth muscle cells associated with hypertension was studied in deoxycorticosterone (DOC)-salt treated rats. Six-week treatment with DOC-salt resulted in significant increases in systolic blood pressure, heart weight, and aortic weight in treated animals compared to increases in uninephrectomized controls. Additionally, the percentage of tetraploid nuclei in aortic smooth muscle cells increased to 17.0 +/- 0.2% in DOC-salt treated rats versus 7.8 +/- 0.3% in normotensive controls. Administration of propranolol (500 mg/L in drinking water) did not inhibit the development of hypertension for up to 4 weeks or the associated increase in cardiac or aortic weight in DOC-salt-treated rats, but did prevent the increase in polyploidy of aortic smooth muscle cell nuclei (8.9 +/- 0.9% in propranolol-treated rats compared to 7.8 +/- 0.3% in normotensive controls). These results indicate that propranolol inhibits the development of hypertension-induced polyploidy in aortic smooth muscle cells of DOC-salt-treated rats and that factors other than blood pressure may be important in this change.

Animals↗
PubMed1988

Does smooth muscle cell polyploidy occur in resistance vessels of spontaneously hypertensive rats?

The ploidy of smooth muscle cells (SMCs) enzymatically isolated from the aorta and superior mesenteric artery (elastic arteries), caudal artery (small muscular artery) and the small mesenteric arteries and arterioles (mesenteric resistance vessels) of the spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats at ages 12, 26, 32 and 40 weeks was determined by flow cytometric DNA analysis and Feulgen-DNA photometric measurements. Frequency of polyploid cells in the aorta and superior mesenteric artery of the SHR increased from 4.43 +/- 1.35 and 7.58 +/- 1.69%, respectively, at 12 weeks to 31.26 +/- 3.00 and 14.13 +/- 1.30% at 40 weeks. There was a smaller increase in the percentage of polyploid cells in these two vessels of the WKY from 4.73 +/- 0.74 and 5.82 +/- 0.33%, respectively, at 12 weeks to 10.64 +/- 0.17 and 7.68 +/- 0.64% at 40 weeks. The caudal artery and mesenteric resistance vessels showed no significant increase in the percentage of 4N (tetraploid) cells in the SHR from 12 weeks (6.80 +/- 0.92 and 6.10 +/- 0.75%) to 40 weeks (7.83 +/- 0.67 and 7.57 +/- 0.07%). Similarly, there was no significant change in ploidy in these arteries of the WKY. Hence, while polyploidy of SMCs increases in the aorta and superior mesenteric artery of the rat with increasing age and with duration of hypertension, there is no significant change in the number of polyploid cells in smaller vessels such as the caudal artery or mesenteric resistance vessels. Since it is the resistance vessels that are involved in the development and maintenance of hypertension, polyploidy of SMCs in the blood vessel wall appears to hold little relevance to the etiology of this disease. As well, increased incidence of polyploidy is not directly attributable to increases in blood pressure as the caudal artery has a high systolic pressure in the SHR yet the incidence of polyploid cells in this artery does not differ from that of the WKY.

Aging↗
PubMed1979

[Polyploidizing mitoses and the biological meaning of polyploidy in liver cells].

The ontogenetic polyploidization of hepatocytes is regarded, within which normal mitoses are changed to polyploidizing mitoses, and diploid hepatocytes transform into polyploid mono- and binuclear cells. A new hypothesis is put forward of the biological significance of the liver cell polyploidy. The hypothesis takes into account a high level of spontaneous chromosomal aberrations in mitotic hepatocytes. The chromosome structural changes interfere with mitosis resulting in the chromosomal imbalance. Polyploidy bestows for hepatocytes a tolerance towards a chromosomal imbalance. Some implications of the hypothesis are discussed: unbalanced genome of hepatocytes after the treatment with mutagens and mitotic stimulators; the reasons of liver cell polyploidy differences in mammalian species; mechanisms of radioresistance of hepatocytes. Chromosomal imbalance of polyploid hepatocytes is assumed to be the basis for wome chronic liver diseases in man.

Animals↗
PubMed1985

[Proliferative response of the arterial wall in arterial hypertension: hyperplasia versus polyploidy].

Proliferation changes are along with cell hypertrophy and extracellular deposit the major components of the hypertensive structural changes in large arteries. There is still some doubt about the nature of the proliferative changes: hyperplasia or polyploidization. The aorta and the tail artery of SHR and Goldblatt one-kidney, one clip hypertensive rats (RVHR) were studied at different ages and hypertensive stages. After enzymatic dispersion, cell relative DNA content was assayed by flow cytofluorimetry and by Feulgen microdensitometry. Tissue total DNA content was assayed by fluorimetry. The increase in diploid and tetraploid cells within the hypertensive arteries was further calculated. In the RVHR, hypertension is of very rapid onset and reaches a plateau within 20 days (compared to the normotensive Wistar, systolic BP is 32 mmHg at 15 days, 52 mmHg at 40 days, 45 mmHg at 90 days). An increase in total aortic DNA content (DNA: 32 micrograms at 15 days, 31 micrograms at 40 days, 40 micrograms at 90 days) is found before the development of a significant polyploidy (polyploidy in per cent: 2.3 p. 100 at 15 and 40 days; 12.0 p. 100 at 90 days). Proliferation changes in this model appears to be hyperplasia at the acute phase and polyploidy at the chronic phase. The course of hypertension is slower and less severe in the SHR (compared to the WKY, systolic BP: 0 mmHg in 4 weeks, 17 mmHg in 8 weeks old and 33 mmHg in 35 weeks old rats).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Factors affecting the incidence of polyploidy in a human in vitro fertilization program.

OBJECTIVE: To study the factors affecting the incidence of polyploidy in an assisted reproduction program. DESIGN: Retrospective analysis. SETTING: University-based subfertility clinic. PATIENTS AND METHODS: Subfertile patients were treated in 163 treatment cycles of in vitro fertilization (IVF) or pronuclear stage tubal transfer (PROST). The relationship between the incidence of polyspermy and the indication of subfertility, the stimulation protocol, the oocyte, and the semen parameters were analyzed. RESULTS: Eighty-nine of the 1,149 oocytes were polyploid (7.8%). The incidence of polyploidy was not affected by the indication for IVF, the age of the patients, the stimulation protocol, the maturity of oocytes as assessed by the appearance of the cumulus, the sperm concentration, the number of sperm inseminated, the serum estradiol level, and the number of oocytes retrieved. The incidence was increased when: (1) the serum estradiol fell before the administration of human chorionic gonadotrophin; (2) the oocyte retrieval-insemination interval was 6 hours or more; (3) the sperm motility was 70% or more; (4) the percentage of sperm with normal morphology was 50% or more. CONCLUSION: The incidence of polyploidy was affected by the serum estradiol pattern, the preinsemination interval, sperm motility, and percentage of morphologically normal sperm.

Adult↗
PubMed1998

Increased polyploidy, delayed mitosis and reduced protein phosphatase-1 activity associated with excess copper in the Long Evans Cinnamon rat.

Until now, it is not known whether copper hepatotoxicity impairs mitosis. Enlarged hepatocytes with huge nuclei considered as polyploids are frequently observed in the Long Evans Cinnamon (LEC) rat which exhibits an abnormal accumulation of hepatic copper due to a defect in the gene homologous to human Wilson's disease gene responsible for intracellular copper delivery. This defect may lead to a abnormal mitotic progression in increased polyploidization and is associated with excessive hepatic copper. This study was designed to examine whether excess copper impairs mitotic progression and results in increased polyploidization using a model of LEC rat liver. Polyploidy was analyzed by flow cytometry. The rate of mitotic progression was investigated using the fraction of mitotic hepatocytes or a mitosis-specific phosphoprotein retained in regeneration. Nuclear protein phosphatase-1 (PP-1) activity essential to mitotic progression was measured. The effect of excess copper on incidence of polyploidy, the rate of mitotic progression and nuclear PP-1 activity was investigated using age- or copper overload-dependent changes in them in LEC rat, or genetic profile-dependent changes of them in backcrosses. LEC rat liver showed an increase of polyploidy, a delay of mitotic progression, and a reduction of nuclear PP-1 activity. These abnormal features concurred with increase of copper concentration accompanied by changes of age in LEC rats from 2 to 4 months of age, induced by dietary copper overload in LEC rat, or caused by single genetic defect in backcrosses. Excess copper impairs mitotic progression, resulting in increased polyploidization. Nuclear PP-1 activity is likely to be at least one of targets of copper hepatotoxicity leading to impairment of mitotic progression.

Age Factors↗
PubMed2005

Nuclear DNA variation, chromosome numbers and polyploidy in the endemic and indigenous grass flora of New Zealand.

BACKGROUND AND AIMS: Little information is available on DNA C-values for the New Zealand flora. Nearly 85 % of the named species of the native vascular flora are endemic, including 157 species of Poaceae, the second most species-rich plant family in New Zealand. Few C-values have been published for New Zealand native grasses, and chromosome numbers have previously been reported for fewer than half of the species. The aim of this research was to determine C-values and chromosome numbers for most of the endemic and indigenous Poaceae from New Zealand. SCOPE: To analyse DNA C-values from 155 species and chromosome numbers from 55 species of the endemic and indigenous grass flora of New Zealand. KEY RESULTS: The new C-values increase significantly the number of such measurements for Poaceae worldwide. New chromosome numbers were determined from 55 species. Variation in C-value and percentage polyploidy were analysed in relation to plant distribution. No clear relationship could be demonstrated between these variables. CONCLUSIONS: A wide range of C-values was found in the New Zealand endemic and indigenous grasses. This variation can be related to the phylogenetic position of the genera, plants in the BOP (Bambusoideae, Oryzoideae, Pooideae) clade in general having higher C-values than those in the PACC (Panicoideae, Arundinoideae, Chloridoideae + Centothecoideae) clade. Within genera, polyploids typically have smaller genome sizes (C-value divided by ploidy level) than diploids and there is commonly a progressive decrease with increasing ploidy level. The high frequency of polyploidy in the New Zealand grasses was confirmed by our additional counts, with only approximately 10 % being diploid. No clear relationship between C-value, polyploidy and rarity was evident.

Cell Nucleus↗
PubMedDate not supplied

Endoreduplication and polyploidy in fragile X cells induced by methotrexate and fluorodeoxyuridine: implications for diagnosis.

Lymphoblastoid cell lines from fragile X patients and amniotic cells from fragile X embryos, when cultured with methotrexate (MTX) or fluorodeoxyuridine (FUdR), showed a significant increase in endoreduplication and polyploidy. This phenomenon was not observed in fragile X lymphocytes or in lymphoblastoid cell lines and amniotic cells of normal control individuals. The relationship between the inducible fragile site at Xq27.3 and the inducible endoreduplication is discussed. The induction of endoreduplication and polyploidy in fragile X lymphoblasts and amniocytes is evaluated as a possible diagnostic test.

Amniotic Fluid↗
PubMed1999

Molecular basis to understand polyploidy.

Polyploidy which is defined as an increase in chromosome number by an exact multiple of the haploid chromosome number is a typical characteristic of plant species but can also be found in almost all organisms from protists to humans. In the plant kingdom, since the reproduction can occur vegetatively, polyploid cells have time to settle down from the evolution point of view as a stable genetic system. So, 30 to 70% of angiosperms, including many important crop plants, are estimated to have polyploidy in their lineages. The success of polyploid species in plants has been attributed to their ability to colonise a wider range of habitats and to survive better in unstable climates compared with their diploid progenitors, presumably due to increased heterozygosity and flexibility provided by the presence of additional alleles.

Animals↗
PubMed2006

Light-dependent polyploidy control by a CUE protein variant in Arabidopsis.

Endoreduplication is a special cell cycle that increases ploidy without cell and nuclear division. In plants endoreduplication is essential for development. We isolated a dominant Arabidopsis mutant from activation tagging lines that had increased polyploidy in darkness. This mutant, ipd1-1D (increased polyploidy level in darkness 1-1D), shows longer hypocotyls and increased ploidy levels only in dark-grown seedlings. The corresponding gene encodes a protein that contains a CUE domain variant. IPD1 is specifically expressed in mitotically dividing cells. Furthermore we show that blue and far-red light can suppress the ploidy increase in ipd1-1D and also suppress the reporter expression in IPD1-promoter beta-glucuronidase transgenic plants. These results suggest that IPD1 regulates the endocycle leading to hypocotyl elongation and this function is controlled by blue and far-red light.

Amino Acid Sequence↗