Nickel(ii) inhibits the oxidation of DNA 5-methylcytosine in mammalian somatic cells and embryonic stem cells

Metallomics ◽  
2018 ◽  
Vol 10 (3) ◽  
pp. 504-512 ◽  
Author(s):  
Ruichuan Yin ◽  
Jiezhen Mo ◽  
Jiayin Dai ◽  
Hailin Wang
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Mammalian Cells ◽  
Somatic Cells ◽  
Embryonic Stem ◽  
Oxidation Of Dna ◽  
Mediated Oxidation

Nickel(ii) inhibits Tet-mediated oxidation of DNA 5-methylcytosine in mammalian cells.

Protecting genomic integrity in somatic cells and embryonic stem cells

2007 ◽  
Vol 614 (1-2) ◽  
pp. 48-55 ◽  
Author(s):  
Y. Hong ◽  
R.B. Cervantes ◽  
E. Tichy ◽  
J.A. Tischfield ◽  
P.J. Stambrook
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Somatic Cells ◽  
Embryonic Stem ◽  
Genomic Integrity

scholarly journals Hybridization of Testis-Derived Stem Cells with Somatic Cells and Embryonic Stem Cells in Mice1

2012 ◽  
Vol 86 (6) ◽  
Author(s):  
Masanori Takehashi ◽  
Masako Tada ◽  
Mito Kanatsu-Shinohara ◽  
Hiroko Morimoto ◽  
Yasuhiro Kazuki ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Somatic Cells ◽  
Embryonic Stem

scholarly journals A p53-dependent response limits the viability of mammalian haploid cells

2017 ◽  
Vol 114 (35) ◽  
pp. 9367-9372 ◽  
Author(s):  
Teresa Olbrich ◽  
Cristina Mayor-Ruiz ◽  
Maria Vega-Sendino ◽  
Carmen Gomez ◽  
Sagrario Ortega ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Cell Lines ◽  
Chromosome Segregation ◽  
Mammalian Cells ◽  
Embryonic Stem ◽  
Myelogenous Leukemia ◽  
Unstable State ◽  
Haploid Cell ◽  
Diploid Cells

The recent development of haploid cell lines has facilitated forward genetic screenings in mammalian cells. These lines include near-haploid human cell lines isolated from a patient with chronic myelogenous leukemia (KBM7 and HAP1), as well as haploid embryonic stem cells derived from several organisms. In all cases, haploidy was shown to be an unstable state, so that cultures of mammalian haploid cells rapidly become enriched in diploids. Here we show that the observed diploidization is due to a proliferative disadvantage of haploid cells compared with diploid cells. Accordingly, single-cell–sorted haploid mammalian cells maintain the haploid state for prolonged periods, owing to the absence of competing diploids. Although the duration of interphase is similar in haploid and diploid cells, haploid cells spend longer in mitosis, indicative of problems in chromosome segregation. In agreement with this, a substantial proportion of the haploids die at or shortly after the last mitosis through activation of a p53-dependent cytotoxic response. Finally, we show that p53 deletion stabilizes haploidy in human HAP1 cells and haploid mouse embryonic stem cells. We propose that, similar to aneuploidy or tetraploidy, haploidy triggers a p53-dependent response that limits the fitness of mammalian cells.

Effect of BMP4 preceded by retinoic acid and co-culturing ovarian somatic cells on differentiation of mouse embryonic stem cells into oocyte-like cells

2015 ◽  
Vol 57 (5) ◽  
pp. 378-388 ◽  
Author(s):  
Soghra Bahmanpour ◽  
Nehleh Zarei Fard ◽  
Tahereh Talaei-Khozani ◽  
Ahmad Hosseini ◽  
Tahereh Esmaeilpour
Keyword(s):  
Stem Cells ◽  
Retinoic Acid ◽  
Embryonic Stem Cells ◽  
Somatic Cells ◽  
Embryonic Stem ◽  
Mouse Embryonic Stem Cells

scholarly journals The Co-Injection of Somatic Cells with Embryonic Stem Cells Affects Teratoma Formation and the Properties of Teratoma-Derived Stem Cell-Like Cells

PLoS ONE ◽  
2014 ◽  
Vol 9 (9) ◽  
pp. e105975 ◽  
Author(s):  
Seung Pyo Gong ◽  
Boyun Kim ◽  
Hyo Sook Kwon ◽  
Woo Sub Yang ◽  
Jae-Wook Jeong ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Embryonic Stem Cells ◽  
Somatic Cells ◽  
Embryonic Stem ◽  
Teratoma Formation

scholarly journals Genome-Wide Reprogramming in Hybrids of Somatic Cells and Embryonic Stem Cells

Stem Cells ◽  
2007 ◽  
Vol 25 (5) ◽  
pp. 1104-1113 ◽  
Author(s):  
Dominic J. Ambrosi ◽  
Borko Tanasijevic ◽  
Anupinder Kaur ◽  
Craig Obergfell ◽  
Rachel J. O'Neill ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Somatic Cells ◽  
Embryonic Stem ◽  
Genome Wide

scholarly journals Citrinin induces apoptosis via a mitochondria-dependent pathway and inhibition of survival signals in embryonic stem cells, and causes developmental injury in blastocysts

2007 ◽  
Vol 404 (2) ◽  
pp. 317-326 ◽  
Author(s):  
Wen-Hsiung Chan
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Mammalian Cells ◽  
Cell Injury ◽  
Reactive Oxygen Species Generation ◽  
Embryonic Stem ◽  
Subsequent Development ◽  
Cytochrome C Release

The mycotoxin CTN (citrinin), a natural contaminant in foodstuffs and animal feeds, has cytotoxic and genotoxic effects on various mammalian cells. CTN is known to cause cell injury, including apoptosis, but the precise regulatory mechanisms of CTN action, particularly in stem cells and embryos, are currently unclear. In the present paper, I report that CTN has cytotoxic effects on mouse embryonic stem cells and blastocysts, and is associated with defects in their subsequent development, both in vitro and in vivo. Experiments in embryonic stem cells (ESC-B5) showed that CTN induces apoptosis via ROS (reactive oxygen species) generation, increased Bax/Bcl-2 ratio, loss of MMP (mitochondrial membrane potential), induction of cytochrome c release, and activation of caspase 3. In this model, CTN triggers cell death via inactivation of the HSP90 [a 90 kDa isoform of the HSP (heat-shock protein) family proteins]/multichaperone complex and subsequent degradation of Ras and Raf-1, further inhibiting anti-apoptotic processes, such as the Ras→ERK (extracellular-signal-regulated kinase) signal transduction pathway. In addition, CTN causes early developmental injury in mouse ESCs and blastocysts in vitro. Lastly, using an in vivo mouse model, I show that consumption of drinking water containing 10 μM CTN results in blastocyst apoptosis and early embryonic developmental injury. Collectively, these findings show for the first time that CTN induces ROS and mitochondria-dependent apoptotic processes, inhibits Ras→ERK survival signalling via inactivation of the HSP90/multichaperone complex, and causes developmental injury in vivo.

Reprogramming of Somatic Cells After Fusion With Induced Pluripotent Stem Cells and Nuclear Transfer Embryonic Stem Cells

2010 ◽  
Vol 19 (2) ◽  
pp. 239-246 ◽  
Author(s):  
Huseyin Sumer ◽  
Karen L. Jones ◽  
Jun Liu ◽  
Corey Heffernan ◽  
Pollyanna A. Tat ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Induced Pluripotent Stem Cells ◽  
Pluripotent Stem Cells ◽  
Nuclear Transfer ◽  
Somatic Cells ◽  
Embryonic Stem ◽  
Induced Pluripotent

scholarly journals Transcriptional repression by FACT is linked to regulation of chromatin accessibility at the promoter of ES cells

2018 ◽  
Vol 1 (3) ◽  
pp. e201800085 ◽  
Author(s):  
Constantine Mylonas ◽  
Peter Tessarz
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Rna Polymerase Ii ◽  
Cell Fate ◽  
Transcription Start Site ◽  
Mammalian Cells ◽  
Es Cells ◽  
Embryonic Stem ◽  
Start Site ◽  
Transcription Start

The conserved and essential histone chaperone, facilitates chromatin transcription (FACT), reorganizes nucleosomes during DNA transcription, replication, and repair and ensures both efficient elongation of RNA Pol II and nucleosome integrity. In mammalian cells, FACT is a heterodimer, consisting of SSRP1 and SUPT16. Here, we show that in contrast to yeast, FACT accumulates at the transcription start site of genes reminiscent of RNA polymerase II profile. Depletion of FACT in mouse embryonic stem cells leads to deregulation of developmental and pro-proliferative genes concomitant with hyper-proliferation of mES cells. Using MNase-seq, Assay for Transposase-Accessible Chromatin sequencing, and nascent elongating transcript sequencing, we show that up-regulation of genes coincides with loss of nucleosomes upstream of the transcription start site and concomitant increase in antisense transcription, indicating that FACT impacts the promoter architecture to regulate the expression of these genes. Finally, we demonstrate a role for FACT in cell fate determination and show that FACT depletion primes embryonic stem cells for the neuronal lineage.

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