Polysomaty and somatic reduction in Phaseolus coccineus L.

By means of karyological, cytophotometric, and autoradiographic analyses it has been shown that, owing to alterations in the DNA synthesis – mitosis sequence, cells with different nuclear conditions are continuously formed de novo and proliferate in Phaseolus coccineus meristems. Besides diploid cells, the following also occur: (i) polyploid cells as the result of chromosome endoreduplication followed by mitosis; (ii) haploid cells as the result of the separation of the two groups of homologous chromosomes in cells that have omitted DNA reduplication; and (iii) since haploid cells undergo chromosome endoreduplication and divide, isogenic cells can be produced. Diploid mitoses alone are present in the meristems of early embryos; haploid mitoses first appear in both root and shoot meristems with increasing embryo development, followed later by cells undergoing chromosome endoreduplication. The study of the root apex has shown that neither polyploid nor reduced cells occur with the same frequency in its various portions. These results are discussed in relation to pertinent data in the literature and the mechanisms responsible for the occurrence of polysomaty and somatic reduction are suggested.Key words: isogenic cells, Phaseolus coccineus, polysomaty, somatic reduction.

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Allelic H3K27me3 to allelic DNA methylation switch maintains noncanonical imprinting in extraembryonic cells

Science Advances ◽

10.1126/sciadv.aay7246 ◽

2019 ◽

Vol 5 (12) ◽

pp. eaay7246 ◽

Cited By ~ 12

Author(s):

Zhiyuan Chen ◽

Qiangzong Yin ◽

Azusa Inoue ◽

Chunxia Zhang ◽

Yi Zhang

Keyword(s):

Dna Methylation ◽

De Novo ◽

Genetic Manipulation ◽

Paternal Allele ◽

Gene Promoters ◽

Maternal Allele ◽

Mammalian Development ◽

Placental Development ◽

Early Embryos ◽

Allele Specific

Faithful maintenance of genomic imprinting is essential for mammalian development. While germline DNA methylation–dependent (canonical) imprinting is relatively stable during development, the recently found oocyte-derived H3K27me3-mediated noncanonical imprinting is mostly transient in early embryos, with some genes important for placental development maintaining imprinted expression in the extraembryonic lineage. How these noncanonical imprinted genes maintain their extraembryonic-specific imprinting is unknown. Here, we report that maintenance of noncanonical imprinting requires maternal allele–specific de novo DNA methylation [i.e., somatic differentially methylated regions (DMRs)] at implantation. The somatic DMRs are located at the gene promoters, with paternal allele–specific H3K4me3 established during preimplantation development. Genetic manipulation revealed that both maternal EED and zygotic DNMT3A/3B are required for establishing somatic DMRs and maintaining noncanonical imprinting. Thus, our study not only reveals the mechanism underlying noncanonical imprinting maintenance but also sheds light on how histone modifications in oocytes may shape somatic DMRs in postimplantation embryos.

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The expanding implications of polyploidy

The Journal of Cell Biology ◽

10.1083/jcb.201502016 ◽

2015 ◽

Vol 209 (4) ◽

pp. 485-491 ◽

Cited By ~ 89

Author(s):

Kevin P. Schoenfelder ◽

Donald T. Fox

Keyword(s):

Cell Size ◽

Recent Progress ◽

Environmental Stresses ◽

Polyploid Cells ◽

Diploid Cells ◽

Metabolic Output

Polyploid cells, which contain more than two genome copies, occur throughout nature. Beyond well-established roles in increasing cell size/metabolic output, polyploidy can also promote nonuniform genome, transcriptome, and metabolome alterations. Polyploidy also frequently confers resistance to environmental stresses not tolerated by diploid cells. Recent progress has begun to unravel how this fascinating phenomenon contributes to normal physiology and disease.

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Transcriptome analysis of tetraploid cells identifies cyclin D2 as a facilitator of adaptation to genome doubling in the presence of p53

Molecular Biology of the Cell ◽

10.1091/mbc.e16-05-0268 ◽

2016 ◽

Vol 27 (20) ◽

pp. 3065-3084 ◽

Cited By ~ 25

Author(s):

Tamara A. Potapova ◽

Christopher W. Seidel ◽

Andrew C. Box ◽

Giulia Rancati ◽

Rong Li

Keyword(s):

Gene Expression ◽

Transcriptome Analysis ◽

Cell Cycle Progression ◽

Target Genes ◽

Single Cells ◽

Cyclin D2 ◽

Genome Doubling ◽

Polyploid Cells ◽

Diploid Cells ◽

P53 Target Genes

Tetraploidization, or genome doubling, is a prominent event in tumorigenesis, primarily because cell division in polyploid cells is error-prone and produces aneuploid cells. This study investigates changes in gene expression evoked in acute and adapted tetraploid cells and their effect on cell-cycle progression. Acute polyploidy was generated by knockdown of the essential regulator of cytokinesis anillin, which resulted in cytokinesis failure and formation of binucleate cells, or by chemical inhibition of Aurora kinases, causing abnormal mitotic exit with formation of single cells with aberrant nuclear morphology. Transcriptome analysis of these acute tetraploid cells revealed common signatures of activation of the tumor-suppressor protein p53. Suppression of proliferation in these cells was dependent on p53 and its transcriptional target, CDK inhibitor p21. Rare proliferating tetraploid cells can emerge from acute polyploid populations. Gene expression analysis of single cell–derived, adapted tetraploid clones showed up-regulation of several p53 target genes and cyclin D2, the activator of CDK4/6/2. Overexpression of cyclin D2 in diploid cells strongly potentiated the ability to proliferate with increased DNA content despite the presence of functional p53. These results indicate that p53-mediated suppression of proliferation of polyploid cells can be averted by increased levels of oncogenes such as cyclin D2, elucidating a possible route for tetraploidy-mediated genomic instability in carcinogenesis.

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Polyploidy in the adult Drosophila brain

10.1101/852723 ◽

2019 ◽

Author(s):

Shyama Nandakumar ◽

Olga Grushko ◽

Laura A. Buttitta

Keyword(s):

Dna Damage ◽

Cell Death ◽

Protective Role ◽

Adult Brain ◽

Exogenous Dna ◽

Damage Response ◽

Polyploid Cells ◽

Drosophila Brain ◽

Accumulation Of Damage ◽

Diploid Cells

AbstractLong-lived cells such as terminally differentiated postmitotic neurons and glia must cope with the accumulation of damage over the course of an animal’s lifespan. How long-lived cells deal with ageing-related damage is poorly understood. Here we show that polyploid cells accumulate in the ageing adult fly brain and that polyploidy protects against DNA damage-induced cell death. Multiple types of neurons and glia that are diploid at eclosion, become polyploid with age in the adult Drosophila brain. The optic lobes exhibit the highest levels of polyploidy, associated with an elevated DNA damage response in this brain region with age. Inducing oxidative stress or exogenous DNA damage leads to an earlier onset of polyploidy, and polyploid cells in the adult brain are more resistant to DNA damage-induced cell death than diploid cells. Our results suggest polyploidy may serve a protective role for neurons and glia in ageing Drosophila melanogaster brains.

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Developmental Genome-Wide DNA Methylation Asymmetry Between Mouse Placenta and Embryo

10.1101/718247 ◽

2019 ◽

Author(s):

LM Legault ◽

K Doiron ◽

A Lemieux ◽

M Caron ◽

D Chan ◽

...

Keyword(s):

Dna Methylation ◽

De Novo ◽

Prenatal Development ◽

Methyltransferase Activity ◽

Developmental Program ◽

Genome Wide ◽

Early Embryos ◽

Somatic Tissues ◽

Main Driver ◽

Methylation Patterns

ABSTRACTIn early embryos, DNA methylation is remodelled to initiate the developmental program but for mostly unknown reasons, methylation marks are acquired unequally between embryonic and placental cells. To better understand this, we generated high-resolution DNA methylation maps of mouse mid-gestation (E10.5) embryo and placenta. We uncovered specific subtypes of differentially methylated regions (DMRs) that contribute directly to the developmental asymmetry existing between mid-gestation embryonic and placental DNA methylation patterns. We show that the asymmetry occurs rapidly during the acquisition of marks in the post-implanted conceptus (E3.5-E6.5), and that these patterns are long-lasting across subtypes of DMRs throughout prenatal development and in somatic tissues. We reveal that at the peri-implantation stages, the de novo methyltransferase activity of DNMT3B is the main driver of methylation marks on asymmetric DMRs, and that DNMT3B can largely compensate for lack of DNMT3A in the epiblast and extraembryonic ectoderm, whereas DNMT3A can only partially compensate in the absence of DNMT3B. However, as development progresses and as DNMT3A becomes the principal de novo methyltransferase, the compensatory DNA methylation mechanism of DNMT3B on DMRs becomes less effective.

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Polyploidy in the adult Drosophila brain

eLife ◽

10.7554/elife.54385 ◽

2020 ◽

Vol 9 ◽

Author(s):

Shyama Nandakumar ◽

Olga Grushko ◽

Laura A Buttitta

Keyword(s):

Dna Damage ◽

Cell Death ◽

Protective Role ◽

Adult Brain ◽

Exogenous Dna ◽

Damage Response ◽

Polyploid Cells ◽

Drosophila Brain ◽

Accumulation Of Damage ◽

Diploid Cells

Long-lived cells such as terminally differentiated postmitotic neurons and glia must cope with the accumulation of damage over the course of an animal’s lifespan. How long-lived cells deal with ageing-related damage is poorly understood. Here we show that polyploid cells accumulate in the adult fly brain and that polyploidy protects against DNA damage-induced cell death. Multiple types of neurons and glia that are diploid at eclosion, become polyploid in the adult Drosophila brain. The optic lobes exhibit the highest levels of polyploidy, associated with an elevated DNA damage response in this brain region. Inducing oxidative stress or exogenous DNA damage leads to an earlier onset of polyploidy, and polyploid cells in the adult brain are more resistant to DNA damage-induced cell death than diploid cells. Our results suggest polyploidy may serve a protective role for neurons and glia in adult Drosophila melanogaster brains.

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P-glycoprotein expression in plasma-cell myeloma is associated with resistance to VAD

Blood ◽

10.1182/blood.v74.3.913.913 ◽

1989 ◽

Vol 74 (3) ◽

pp. 913-917 ◽

Cited By ~ 114

Author(s):

J Epstein ◽

HQ Xiao ◽

BK Oba

Keyword(s):

Nuclear Dna ◽

De Novo ◽

Disease Process ◽

Nuclear Dna Content ◽

Clinical Implications ◽

Systematic Analysis ◽

Resistant Disease ◽

P Glycoprotein ◽

Aneuploid Tumor ◽

Diploid Cells

Abstract Tumor cell-associated expression of multidrug resistance (MDR) was quantitated in 22 patients with DNA-aneuploid myeloma using 2-parameter flow cytometry with monoclonal antibody (MoAb) C-219 for the detection of cytoplasmic p-170 and propidium iodide for nuclear DNA content. The proportion of cells expressing p-170 and the intensity of p-170-related fluorescence were determined for each patient. Among the 14 patients treated with vincristine-adriamycin-dexamethasone (VAD), the proportion of p-170-positive cells distinguished sensitive from resistant disease (P less than .01). Among a subgroup of seven patients with MDR analysis available prior to VAD therapy, two subsequent nonresponders had high proportions of C-219-reactive cells. The presence de novo of high proportions of p-170-expressing cells in another still untreated patient and in a further individual with resistance to dexamethasone and interferon (not associated with MDR) warrants systematic analysis of p-170 expression prior to therapy to determine its clinical implications for response to MDR-associated drugs as combined in the VAD regimen. Concurrent MDR expression by aneuploid tumor cells and cells in the diploid subcompartment may represent involvement of diploid cells in the myeloma disease process.

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Pairing competition between identical and homologous chromosomes in diploid and tetraploid cells of rye telotrisomic plants

Canadian Journal of Genetics and Cytology ◽

10.1139/g86-083 ◽

1986 ◽

Vol 28 (4) ◽

pp. 568-573 ◽

Cited By ~ 4

Author(s):

E. Benavente ◽

J. Orellana

Keyword(s):

Secale Cereale ◽

Homologous Chromosomes ◽

Diploid Cells

Pairing competition between identical and homologous chromosomes 1R has been directly analyzed in diploid–tetraploid chimeras of telotrisomic plants of rye Secale cereale by using C-bands as cytological markers. The results have shown pairing preferences either in diploid cells, with three doses of 1RS, and in tetraploid cells, with six doses. In both cases, the preferences found could be explained by differential pairing affinities between chromosomes.Key words: telotrisomic, rye, chimeras, banding (C), pairing.

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