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PubMed2001

Documentation of normal and leukemic myelopoietic progenitor cells with high-resolution phase-contrast time-lapse cinematography.

The high-resolution phase-contrast, time-lapse cinematography using oil immersion lenses and 16-mm film demonstrates the kinetic cell events as maturation, locomotion, mitosis, and apoptosis of cells cultivated at 37 degrees C for up to 10 days. 0.5 v/v frozen-thawed sera with presumably high cytokine concentrations were added to the plasma or agar clot. Vital progenitor cells from human bone marrow and blood have a large, bright, unstructured nucleus with a large nucleolus and a narrow rim of cytoplasm (nuclear/cytoplasmic volume ratio = 0.7). Their nuclei are 6-14 micrometer in diameter and double their volume within 8 h. Many (70%) move at a mean speed of 2 micrometer/min, and many (30%) multiply with alpha-2alpha mitoses, generating progenitor cell families. Various disturbances during the course of mitosis lead to the formation of polyploid cells, thereby yielding the megakaryocytic cell line. Some of the progenitor cells undergo asymmetric alpha-alphan mitoses: One of the two initially identical daughter cells remains a progenitor cell in the morphological sense, whereas the other daughter cell - depending on the size of its mother cell - matures in the same culture medium to form a granulocytopoietic, monocytopoietic or erythrocytopoietic cell line. - In acute myeloid leukemias (AML), the blasts and their nuclei are slightly larger than the corresponding progenitor cells and move faster (5 micrometer/min). Symmetric alpha-2alpha mitoses permit unlimited multiplication of the leukemic blasts if contact with cytotoxic lymphocytes does not render them apoptotic. This results in more stromal cells than normal. Granulocytopenia, monocytopenia, and anemia occur due to the genetic impairment of signaling control for asymmetric alpha-alphan mitoses, and thrombocytopenia occurs due to the reduction in polyploidization.

Bone Marrow Cells↗
PubMed1986

Occurrence of premature chromosome condensation in mouse spermatogonia treated with busulfan.

Busulfan induction of premature chromosome condensation (PCC) was examined in mouse spermatogonia. Adult (C3H X SWV) F1 male mice were injected intraperitoneally with busulfan at 10 or 30 mg/kg of body weight and killed 18-72 h later. Polyploid-like mitoses were frequent (ca. 1/4 of all spermatogonial mitoses examined) in both the untreated and treated groups. Most of these were considered to have been derived from normal spermatogonia. In busulfan-treated mice, polyploid-like mitoses with PCC were seen. The frequency of PCC-containing mitoses increased with increasing dose and exposure time. A possible interpretation for PCC induction in mouse spermatogonia is discussed.

Animals↗
PubMed1987

Prognostic value of malignancy grading and DNA measurements in small glottic carcinomas.

Thirty-three small glottic carcinomas (T1 and small T2; UICC, 1978) were examined by malignancy grading using the 8-factor system proposed by Jakobsson et al. [Acta radiol. Ther. phys. Biol. 12: 1-8, 1973] and the 4-factor system set up by Glanz and Eichhorn [Hals-Nas.-Ohrenarzt 33: 103-111, 1985]. DNA ploidy, S-phase, and the presence of polyploid cell nuclei were determined. There was no significant difference in malignancy score or DNA values between tumors that recurred after a full course of radiotherapy and those that did not. All but one carcinoma that recurred had polyploid nuclei, in comparison with only 13 of the 22 nonrecurrent tumors. Neither malignancy grading nor DNA measurements seem to predict the clinical course of small glottic carcinomas. Accurate and adequate radiotherapy may be more reliable for local tumor control than tumor character. The extent of the tumor, such as the involvement of the anterior commissure, may be another factor affecting the prognosis.

Aged↗
PubMed1977

Karyological and electron-microscopic studies in myocardial cells of primates after experimentally induced cardiac hypertrophy.

Precocious polyploidization in hypertrophic hearts of infants with congenital malformation can be reproduced banding the ascending aorta of young rhesus monkeys. Electron micrographs show hypoxic changes, signs of DNA, RNA, and protein synthesis as well as degenerative changes comparable to human hearts. Enforced polyploidization of cor pulmonale is found in rhesus exposed to coal quartz dust for 48 months. The pig heart, containing disturbed mitoses, serves as a model for incomplete mitoses. During evolution they became the rule for the myocardial cells of primates.

Animals↗
PubMed1983

Vascular smooth muscle cell hypertrophy and hyperploidy in the Goldblatt hypertensive rat.

Our major objective in this study was to examine the hypothesis that the aortic smooth muscle cell hypertrophy and hyperploidy observed in previous studies of spontaneously hypertensive rats is not peculiar to that model, but also occurs in Sprague-Dawley rats made hypertensive by a Goldblatt procedure (two-kidney, one-clip model). Flow microfluorometric and microdensitometric analysis of smooth muscle cell DNA content showed a significant increase in the frequency of tetraploid smooth muscle cells from 5.6 +/- 0.9% in controls to 14.6 +/- 1.94% in hypertensives 1 month after Goldblatt surgery. Neither differences in ploidy nor elevation in blood pressure were apparent 2 weeks after surgery. The frequency of polyploid smooth muscle cells increased with age, duration of hypertension, and level of blood pressure. Analysis of the interrelationship between smooth muscle cell ploidy and hypertrophy in 5-month post-surgery Goldblatts by cytospectrophotometric measurements of the protein and DNA content of individual smooth muscle cells showed that tetraploid and octaploid cells from Goldblatt rats had 64% and 129% greater protein mass, respectively, than diploid cells. In addition, the mean protein mass of smooth muscle cells from Goldblatts was approximately 100% greater than that of normotensive controls, with each of the ploidy classes in Goldblatts having a higher frequency and mass than the corresponding cells in controls. Estimates of cell number per centimeter aortic length, based on measurements of average DNA/cell and total aortic medial DNA, showed no difference between hypertensives and controls. Furthermore, the rate of accumulation of polyploid cells could account for the increased frequency of cells undergoing DNA synthesis as measured by [3H]thymidine autoradiography. Thus, smooth muscle cell hypertrophy, not hyperplasia, was responsible for the increased mass of smooth muscle in aortas of Goldblatt hypertensive rats compared with normotensive controls, and this smooth muscle cell hypertrophy was accompanied by an increase in DNA ploidy.

Animals↗
PubMed1985

Differential effects of antihypertensive drug therapy on vascular smooth muscle cell hypertrophy, hyperploidy, and hyperplasia in the spontaneously hypertensive rat.

The present report extends our previous studies of smooth muscle cell hypertrophy, hyperploidy, and hyperplasia in the 5-month-old spontaneously hypertensive and Wistar-Kyoto rats to include analyses of 3- and 7-month-old rats and explores the effects of antihypertensive drug treatment on the accelerated growth of vascular smooth muscle in aortas of spontaneously hypertensive vs. Wistar-Kyoto rats. Drug-treated rats were administered a combination of reserpine, hydralazine, and chlorathiazide in their drinking water, either between 3 and 5 months or between 5 and 7 months of age. Drug treatment decreased the blood pressure of spontaneously hypertensive rats to values at or below those of Wistar-Kyoto rats for both age-treatment groups. Smooth muscle growth was evaluated by morphometric analyses of aortic smooth muscle content, flow cytometric and microdensitometric measurements of the frequency of polyploid smooth muscle cells, biochemical estimates of aortic medial smooth muscle cell number, and microdensitometric measurements of individual smooth muscle cell protein content. The following results were obtained. Aortic medial smooth muscle content was not significantly increased in 3-month spontaneously hypertensive compared to Wistar-Kyoto rats, indicating that aortic smooth muscle hypertrophy occurred post-3 months, as well as after blood pressure was elevated. In 5-month-old spontaneously hypertensive and Wistar-Kyoto rats, medial smooth muscle hypertrophy could be accounted for by cellular hypertrophy without hyperplasia; in contrast, medial hypertrophy in 7-month-old spontaneously hypertensive rats involved both cellular hypertrophy and hyperplasia. Antihypertensive treatment prevented the accelerated growth of vascular smooth muscle that occurred in spontaneously hypertensive rats via cellular hypertrophy and hyperploidy, but it did not prevent an increase in smooth muscle cell number in spontaneously hypertensive rats between 5 and 7 months of age. Furthermore, it had no effect on the parallel increases in aortic medial smooth muscle cell number that occurred in both spontaneously hypertensive and Wistar-Kyoto rats between 3 and 5 months of age. Whereas drug treatment prevented accelerated development of smooth muscle cell polyploidism in spontaneously hypertensive rats, in no case (spontaneously hypertensive or Wistar-Kyoto rats) did it reverse changes in ploidy that existed at the time of initiation of drug treatment, although it did cause cellular atrophy in smooth muscle cells of each ploidy class.(ABSTRACT TRUNCATED AT 400 WORDS)

Age Factors↗
PubMed2004

Megakaryocytes express functional Aurora-B kinase in endomitosis.

Endomitosis (EnM) in megakaryocytes (MKs) is characterized by abortion of mitosis in late anaphase and failure of cytokinesis; subsequent reinitiation of DNA synthesis results in polyploidy. Ablation of chromosomal passenger proteins including Aurora-B kinase causes defects in late anaphase and cytokinesis in diploid cells; thus one hypothesis is that the expression or function of these proteins in polyploid MKs is abnormal. It has been reported that Aurora-B kinase mRNA is decreased in polyploid megakaryocytic cells, suggesting that deficiency of Aurora-B kinase is responsible for EnM. We examined the localization of Aurora-B kinase and additional members of the chromosomal passenger protein and aurora kinase families in MKs. We found that in EnM MKs (1) Aurora-B kinase is present and appropriately localized to centromeres in early EnM; (2) in low-ploidy human MKs, centromeric localization of survivin and inner centromere protein (INCENP) can also be demonstrated; (3) the function of Aurora-B kinase, as measured by Ser10 phosphorylation of histone H3, is intact; and (4) aurora-A kinase localizes appropriately to centrosomes in EnM. These results suggest that EnM MKs appropriately express functional Aurora-B kinase and related proteins in early anaphase, making a simple deficiency of this protein an unlikely explanation for polyploidy in this cell type.

Anaphase↗
PubMed2005

Mammalian target of rapamycin (mTOR) regulates both proliferation of megakaryocyte progenitors and late stages of megakaryocyte differentiation.

A major determinant in platelet production is the megakaryocyte (MK) size that is regulated both by ploidization and the increase in cytoplasmic volume at the end of maturation. Here we investigated the involvement of the mammalian target of rapamycin (mTOR) pathway in the regulation of megakaryopoiesis. We show that phosphorylation of mTOR, p70S6K1, and 4E-BP1 was diminished in thrombopoietin-cultured human MKs after rapamycin treatment. Rapamycin induced an inhibition in the G1/S transition and a decrease in the mean MK ploidy via a diminution of p21 and cyclin D3 occurring at a transcriptional level. Both cycling (2N/4N) and polyploid (8N/16N) MKs were reduced in size, with a size reduction slightly more pronounced in mature polyploid MKs than in immature ones. Rapamycin also induced a delay in the expression of MK markers and prevented the generation of proplatelet MKs. Additional experiments performed in vitro with MKs from mutant mice showed that the decrease in mean ploidy level and the delay in MK differentiation in the presence of rapamycin were less pronounced in CdknIa (p21)-/- MKs than in CdknIa (p21)+/+ MKs. These findings indicate that the mTOR pathway plays an important role during megakaryopoiesis by regulating ploidy, cell size, and maturation, in part by regulating p21 and cyclin D3.

Animals↗
PubMed2002

Different ploidy levels of megakaryocytes generated from peripheral or cord blood CD34+ cells are correlated with different levels of platelet release.

Ploidy could be the key to understanding megakaryocyte (MK) biology and platelet production. Human CD34+ cells purified from umbilical cord blood (CB) and peripheral blood (PB) were investigated on their capability to give rise, in a serum-free medium containing thrombopoietin, to MKs and platelets. CB-MKs showed reduced polyploidization and platelet number compared with PB-MKs, but a similar membrane phenotype. Most CB-MKs showed a 2N content of DNA (approximately 80%) and only 2.6% had 8N, whereas 40% of the PB cells had 8N or more. Platelets were substantially released in PB culture from day 12; at day 14 the CB-derived MKs were able to release platelets although at a reduced level (approximately 35%), correlating with their reduced size. A direct correlation was demonstrated by sorting polyploid cells from PB-MKs and evaluating the platelets released in the supernatant. Furthermore, the study analyzed the expression and distribution of cyclin D3 and cyclin B1. Cyclin D3 protein was increased in PB in comparison to CB-MKs; in PB culture most cells rapidly became positive, whereas in CB-derived cells cyclin D3 expression was evident only from day 9 and in a reduced percentage. Cyclin B1 was essentially localized at the nuclear level in the CB and was expressed during the whole culture. In PB-MKs, at day 9, a reduction was observed, correlating with an advanced ploidy state. The data indicate the inability of the CB-MKs to progress in the endomitotic process and a direct correlation between DNA content and platelet production.

Adult↗
PubMed2006

Microarray expression analysis of meiosis and microsporogenesis in hexaploid bread wheat.

BACKGROUND: Our understanding of the mechanisms that govern the cellular process of meiosis is limited in higher plants with polyploid genomes. Bread wheat is an allohexaploid that behaves as a diploid during meiosis. Chromosome pairing is restricted to homologous chromosomes despite the presence of homoeologues in the nucleus. The importance of wheat as a crop and the extensive use of wild wheat relatives in breeding programs has prompted many years of cytogenetic and genetic research to develop an understanding of the control of chromosome pairing and recombination. The rapid advance of biochemical and molecular information on meiosis in model organisms such as yeast provides new opportunities to investigate the molecular basis of chromosome pairing control in wheat. However, building the link between the model and wheat requires points of data contact. RESULTS: We report here a large-scale transcriptomics study using the Affymetrix wheat GeneChip(R) aimed at providing this link between wheat and model systems and at identifying early meiotic genes. Analysis of the microarray data identified 1,350 transcripts temporally-regulated during the early stages of meiosis. Expression profiles with annotated transcript functions including chromatin condensation, synaptonemal complex formation, recombination and fertility were identified. From the 1,350 transcripts, 30 displayed at least an eight-fold expression change between and including pre-meiosis and telophase II, with more than 50% of these having no similarities to known sequences in NCBI and TIGR databases. CONCLUSION: This resource is now available to support research into the molecular basis of pairing and recombination control in the complex polyploid, wheat.

Chromosome Pairing↗
PubMed2025

Cytotype classification and genetic diversity of Platostoma palustre revealed by rDNA localization and chloroplast genome.

BACKGROUND: Platostoma palustre A. J. Paton is an edible medicinal plant that plays a significant role in traditional food production and medicinal applications. However, the genetic basis of P. palustre remains unclear, thereby hampering research on its genome and polyploid evolution. RESULTS: To characterize the karyotype and ploidy of P. palustre, we performed fluorescence in situ hybridization (FISH) by using 35 S and 5 S rDNA probes in P. palustre. FISH results indicated that 35 S rDNA mapped to the end of the chromosome (chromosome satellite, heterochromatic region) and that 5 S rDNA was located close to the centromere of the chromosomes. Based on the rDNA sites, we identified three distinct cytotypes of P. palustre: diploid (2n = 2x = 30, x = 15), triploid (2n = 3x = 45, x = 15), and tetraploid (2n = 4x = 60, x = 15). To further explore the genetic evolutionary relationship among these P. palustre cytotypes, we conducted Illumina sequencing and assembled the chloroplast (CP) genome. The CP genomes of P. palustre accessions maintained a conserved single circular molecule with a length of 152,534 - 152,788 bp, comprising a large single-copy region (LSC) and small single-copy region (SSC) separated by two inverted repeat regions (IRs). Phylogenetic trees were also created based on CP and nuclear molecular markers, showing that most P. palustre accessions clustered together corresponding to their collection regions. Of these, GDZC2 (2n = 2x = 30) clustered with several triploid accessions, suggesting that it may share a common ancestor with these triploid accessions. CONCLUSIONS: This is the first study to characterize the karyotype, identify three cytotypes of P. palustre using FISH, and provide molecular evidence for an evolutionary relationship among different P. palustre accessions. These findings will be useful for further genomic studies and polyploid evolution of P. palustre.

Genome, Chloroplast↗
PubMed1984

Uterine deoxyribonucleic acid synthesis during preimplantation in precursors of stromal cell differentiation during decidualization.

During early pseudopregnancy, DNA synthesis and mitosis in the uterine endometrial stroma precede the development of uterine sensitivity to deciduogenic stimuli. Progesterone redirects the effects of estradiol on endometrial DNA synthesis from the luminal epithelium to the stroma. To determine the time and hormonal control of preimplantation endometrial DNA synthesis, uterine cells were labeled with [3H] thymidine at specific times during early pseudopregnancy or after progestin and estrogen treatment of ovariectomized rats. The fate of these labeled cells after their decidualization was examined by separation of prelabeled deciduomal cells by velocity sedimentation at unit gravity, which separates cells by size. Stromal cells that synthesized DNA during early pseudopregnancy or in response to hormone treatment later differentiated into deciduomal cells. Rates of DNA synthesis increased on days 4 and 5 of pseudopregnancy, with greater incorporation occurring on day 4 in cells that differentiated into polyploid deciduomal cells. In ovariectomized rats, medroxyprogresterone acetate treatment for 15 h increased DNA synthesis in stromal cells that differentiated into diploid and tetraploid deciduomal cells. DNA synthesis increased further at 30 h before returning to basal levels at 48 h. After progestin pretreatment, estradiol treatment increased stromal DNA synthesis again with greater incorporation in cells differentiating into polyploid deciduomal cells. These data indicate that during early pseudopregnancy, both progesterone and estradiol control the DNA synthesis of endometrial stromal cells as a means of reprogramming these cells for the later growth and differentiation of decidualization.

Animals↗
PubMed2004

missing oocyte encodes a highly conserved nuclear protein required for the maintenance of the meiotic cycle and oocyte identity in Drosophila.

In Drosophila, a single oocyte develops within a 16-cell germline cyst. Although all 16 cells initiate meiosis and undergo premeiotic S phase, only the oocyte retains its meiotic chromosome configuration and remains in the meiotic cycle. The other 15 cells in the cyst enter the endocycle and develop as polyploid nurse cells. A longstanding goal in the field has been to identify factors that are concentrated or activated in the oocyte, that promote meiotic progression and/or the establishment of the oocyte identity. We present the characterization of the missing oocyte gene, an excellent candidate for a gene directly involved in the differentiation of the oocyte nucleus. The missing oocyte gene encodes a highly conserved protein that preferentially accumulates in pro-oocyte nuclei in early prophase of meiosis I. In missing oocyte mutants, the oocyte enters the endocycle and develops as a polyploid nurse cell. Genetic interaction studies indicate that missing oocyte influences meiotic progression prior to pachytene and may interact with pathways that control DNA metabolism. Our data strongly suggest that the product of the missing oocyte gene acts in the oocyte nucleus to facilitate the execution of the unique cell cycle and developmental programs that produce the mature haploid gamete.

Amino Acid Sequence↗
PubMed1988

Polytene chromosomes in mouse trophoblast giant cells.

Mouse trophoblast giant cells undergo successive rounds of DNA replication resulting in amplification of the genome. It has been difficult to determine whether giant cell chromosomes are polyploid as in liver cells or polytene as in Dipteran salivary glands because the chromosomes do not condense. We have examined the pattern of hybridization of mouse giant cells with a variety of in situ chromosome markers to address this question. Hemizygous markers displayed one hybridization signal per nucleus in both diploid and giant cells, while homozygous markers displayed two signals per nucleus in both cell types. These patterns are consistent with cytological evidence indicating that giant cell chromosomes are polytene rather than polyploid. However, in contrast to the situation in Dipteran salivary glands, the two homologues do not appear to be closely associated. We conclude that the mechanism of giant cell DNA amplification involves multiple rounds of DNA replication in the absence of both karyokinesis and cytokinesis, and that sister chromatids, but not homologous chromosomes, remain closely associated during this process.

Animals↗
PubMed1997

Mutation of a gene for a Drosophila kinesin-like protein, Klp38B, leads to failure of cytokinesis.

Mutations in a gene (Klp38B) encoding a novel kinesin-like protein in Drosophila melanogaster lead to the formation of polyploid cells in the larval central nervous system and in the follicle cells of adult egg chambers. Some homozygous mutants survive to adulthood and also exhibit morphological defects indicative of abnormal cell cycle progression, including rough eyes, missing bristles, and abnormal abdominal cuticles. In larval brains, there is no accumulation of mitotic cells and the frequency of anaphase figures is comparable to wild type, suggesting that nuclear division is not affected. Such brains contain polyploid cells with metaphase and anaphase chromosomes associated with bipolar spindles. Such spindles have a number of unseparated centrosomes at their poles reflecting the degree of polyploidy of the cell. Follicle cells frequently contain two nuclei of roughly equal size. Taken together, we conclude that these Klp38B mutations lead to a failure of cytokinesis resulting in polyploidy, and discuss whether or not this is a direct effect of the mutation.

Amino Acid Sequence↗
PubMed2000

Characterization of cancer cell lines established from two human metastatic breast cancers.

Cell lines are valuable resources for the study of the malignancy and potential therapy of human breast cancer. A major problem with adapting fresh breast tumor specimens to grow in vitro is contamination by fibroblasts. Previously, we have reported a technique to overcome this problem (Nayak, S. K; Dillman, R. O. Clin. Biotechnol. 3:237-242; 1991). We have recently established two new breast cancer cell lines, HH315 and HH375, that were derived from abdominal and supraclavicular lymph node metastases from two patients. They were characterized by (1) growth kinetics; (2) staining with monoclonal antibodies (MoAbs) to cytokeratin-19, epithelial membrane antigen (EMA), anticarcinoembryonic antigen (CEA), breast cancer antigen 1 (BRST-1), breast cancer antigen 2 (BRST-2), Her2/neu, and p53; (3) expression of domains of urinary plasminogen activator (uPA), neural cell adhesion molecule (NCAM), and haptoglobin (Hp) (Harvey et al., 1997); and (4) karyotypic analysis. Growth kinetic studies showed that doubling times for both lines ranged from 48 to 96 h. These two cell lines were found to have characteristics of the metastatic breast cancer cells. Both lines stained positive with MoAbs to cytokeratin-19 and EMA, thus confirming their epithelial origin. They also strongly reacted with the pan-breast carcinoma MoAbs BRST-1 and BRST-2, and carcinoembryonic CEA MoAb. Both cell lines overexpressed the oncogene proteins Her2/neu and p53. The tumor cells were negative for estrogen and progesterone receptors. HH315 cells were poorly differentiated, whereas the HH375 cells exhibited adenocarcinoma morphology. Both cell lines showed intense cell surface and some cytoplasmic staining for uPA, NCAM, and Hp domains, which is a characteristic of malignant neoplasms (Harvey et al., 1997). The HH375 cell line showed two cell types, of which 60% were hyperdiploids with 60-70 chromosomes and 5-10 marker chromosomes. The remaining cells were polyploid with more than 200 chromosomes. Cell line HH315 consisted of only a polyploid population. These cell lines may be useful in breast cancer research.

Breast Neoplasms↗
PubMedDate not supplied

Spontaneous cell transformation: karyoplasts derived from multinucleated cells produce new cell growth in senescent human epithelial cell cultures.

Previously, it was shown that SV40-induced cell transformation of human diploid (2N), epithelial cells was a dynamic process of nuclear and cellular events. In this process, nuclei of polyploid (above 2N) cells broke down into multinucleated cells (MNCs) by amitotic division. An induced mass karyoplast (i.e., small cell with reduced amount of cytoplasm) budding process from the MNCs produced transformed cells with extended life span (EL) and altered morphology. In this study, without the use of SV40 and no induction of karyoplast budding, the same sequence of cellular events was found to occur spontaneously for the same type of cells at replicative senescence (no mitosis). These cell transformation events were followed by phase-contrast photography of living cell cultures. Primary, diploid, epithelial cell cultures grew for two to three passages and then entered senescence. Cells remaining in the cultures after widespread cell death (mortality stage 1; M1) developed the typical large, flat-cell morphology of senescence with increased cytoplasmic volume. Some of these cells were MNCs, mostly with two to four nuclei. Cytokinesis in MNCs and spontaneous karyoplast budding from MNCs were observed, and new, limited EL cell growth was present either in foci of cells or as prolonged cell growth over one to two passages. At the end of their replicative phase, the EL cells entered another death crisis (M2) from which no cells survived. In M2-crisis, rarely transformed cells appear with immortal cell growth characteristics (i.e., cell lines). Numerous examples of fragmentation or amitosis of polyploid nuclei in the production of multinucleated cells (MNCs) are presented. Such nuclear divisions produced nuclei with unequal sizes, which suggest unbalanced chromosomal segregations. The nuclear and cellular events in cell transformation are compared with a natural (no induction) occurrence of MNC-offspring cells in mammalian placentas. The possibility of a connection between these two processes is discussed. And finally the difference in the duration of EL cell growth from SV40-MNCs versus from senescent-MNCs is ascribed to increased mutational load in SV40-induced MNCs as compared with that in senescence MNCs.

Amniocentesis↗
PubMed2004

Rapid changes of microsatellite flanking sequence in the allopolyploidization of new synthesized hexaploid wheat.

It was suggested that the rapid changes of DNA sequence and gene expression occurred at the early stages of allopolyploid formation. In this study, we revealed the microsatellite (SSR) differences between newly formed allopolyploids and their donor parents by using 21 primer sets specific for D genome of wheat. It was indicated that rapid changes had occurred in the "shock" process of the allopolyploid formation between tetraploid wheat and Aegilops tauschii. The changes of SSR flanking sequence resulted in appearance of novel bands or disappearance of parental bands. The disappearance of the parental bands showed much higher frequencies in comparison with that of appearance of novel bands. Disappearance of the parental bands was not random. The frequency of disappearance in tetraploid wheat was much higher than in Ae. tauschii, i. e. the disappearance frequency in AABB genome was much higher than in D genome. Changes of SSR flanking sequence occurred at the early stage of F1 hybrid or just after chromosome doubling. From the above results, it can be inferred that SSR flanking sequence region was very active and was amenable to change in the process of polyploidization. This suggested that SSR flanking sequence probably had special biological function at the early stage of ployploidization. The rapid and directional changes at the early stage of polyploidization might contribute to the rapid evolution of the newly formed allopolyploid and allow the divergent genomes to act in harmony.

Genome, Plant↗