Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA340266 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4069120.fastq.gz | Fastqsanger.gz | |||
| SRR4069121.fastq.gz | Fastqsanger.gz | |||
| SRR4069112.fastq.gz | Fastqsanger.gz | |||
| SRR4069122.fastq.gz | Fastqsanger.gz | |||
| SRR4069113.fastq.gz | Fastqsanger.gz |
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Project description:RNA-Seq analysis of 4N and 2N RPE1 cells following polyploid induction via cytokinesis failure or Aurora kinase inhibition [tpo3]
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Project description:We characterized regions of underrepresentation that are specific to mouse polyploid trophoblast giant cells. We performed array Comparative Genomics Hybridization (aCGH) to examine copy number variation (CNV) in mouse polyploid trophoblast giant cells (TGCs). We performed the following experiments in duplicates to examine CNV during various stages of in vivo and in vitro TGC development: e9.5 TGCs vs. embryonic controls, e11.5 TGCs vs. embryonic controls, e13.5 TGCs vs. embryonic controls, e16.5 TGCs vs. embryonic controls, as well as TGCs cultured 3, 5 and 7 days vs. 2N trophoblast stem cells. We also performed the following controls to show that underrepresentation is only found in polypoid trophoblast giant cells and not in either 2N placental cell types nor in other types of polyploid cells: 2N placenta disk vs. embryonic controls, 2N trophoblast stem cells vs. embryonic stem cells, and polyploid Megakaryocytes vs. embryonic controls. When possible, we performed arrays with the test and control samples of opposite sex (F-female, M-male), as an internal control for the array.
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Project description:This 89-node Boolean model of mammalian growth factor signaling can reproduce oscillations in PI3K signaling in cycling cells, and links these oscillations to the regulatory networks that drive each phase of cell cycle progression, as well as apoptosis. It builds on our previous work on modeling cell cycle progression as the interaction of two linked multi-stable switches (Deritei et al, Sci Rep 6:21957, 2016) and extends it to capture the role of Plk1 in cell cycle progression.
The resulting model reproduces the following experimentally documented cell behaviors:
— cyclic PI3K/AKT1 activity in dividing cells, which remain in sync with the cell cycle
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timing of Plk1 loss; namely, G2 arrest, mitotic catastrophe, premature anaphase and chromosome mis-segregation leading to aneuploidy, and failure to complete cytokinesis following telophase, which can lead to genome duplication
— failure of cytokinesis and accumulation of binucleate telophase cells driven by hyperactive PI3K, hyperactive Ak1, or FoxO inhibition.
— the effect of a large number of knockdown / forced activation mutations
Testable predictions:
— PI3K degradation in response to high PI3K activation is driven by the Neddl4 ubiquitin ligase activated by PLCγ, while its re-synthesis requires nuclear re-accumulation of FoxO3.
— The degradation/re-synthesis cycle of PI3K occurs twice per division cycle, synchronized by Plk1-mediated inhibition of FoxO3 during metaphase/anaphase.
— Cells in which PI3K is inhibited after the start of DNA synthesis can nevertheless pre-commit to another cell cycle in the presence of saturating growth stimulation (passing the restriction point in late metaphase), albeit at lower rates than wild-type cells.
— Cell cycle defects in response to PI3K/Ak1 over-activation or FoxO knockdown are driven by a loss of Plk1 in telophase.
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Project description: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 impact on cell-cycle progression. Acute polyploidy was generated by knockdown of 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 upregulation 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 point out 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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