Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA340267 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4069100.fastq.gz | Fastqsanger.gz | |||
| SRR4069110.fastq.gz | Fastqsanger.gz | |||
| SRR4069101.fastq.gz | Fastqsanger.gz | |||
| SRR4069111.fastq.gz | Fastqsanger.gz | |||
| SRR4069102.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 18 |
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Project description:RNA-Seq analysis of 4N and 2N RPE1 cells following polyploid induction via cytokinesis failure by siRNA knockdown of Anillin [tpo8]
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Project description:RNA-Seq analysis of proliferating 4N and 2N RPE1 cells derived from single cell clones following inhibition of Aurora B to induce polyploidization [tpo10]
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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: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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