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Next Generation Sequencing Quantitative Analysis of Wild Type and Mki67-/- 4T1 mouse mammary carcinoma cell transcriptomes

ABSTRACT: Purpose: The goals of this study were to compare gene expression profiles of mouse 4T1 cells with intact or disrupted Mki67 gene. Methods: mRNA profiles of wild-type (WT) and two clones of Ki-67 knockout (Mki67−/−) mouse NIH/3T3 cells, all in duplicate, were generated by deep sequencing using Illumina Hiseq2500 in single-end read mode, 50bp. The sequence reads that passed quality filters were aligned to the mouse genome, quantified, and differential gene expression (DGE) analysis was performed using DEseq2. Results: Using an optimized data analysis workflow, we mapped about 30 million sequence reads per sample to the mouse genome (GRCm38.p6) and identified differentially expressed genes. This revealed widespread changes in gene expression, with 2558 genes significantly deregulated in independent clones of Mki67-/- cells (q < 0.05) Conclusions: Ki-67 knockout causes genome-scale transcriptome alterations

ORGANISM(S): Mus musculus

PROVIDER: GSE162358 | GEO | 2021/02/18

REPOSITORIES: GEO

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Next Generation Sequencing Quantitative Analysis of the transcriptomes of Wild Type and Mki67-/- 4T1 tumors in mice

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2021-02-18 | GSE162352 | GEO

Next Generation Sequencing Quantitative Analysis of Wild Type and Mki67-/- 4T1 mouse mammary carcinoma cell histone modification

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Gene expression analysis of mouse intestinal cells that lack Cdk8

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2015-07-31 | GSE71385 | GEO

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Project description:Antigen Ki-67 is a nuclear protein expressed in proliferating mammalian cells. It is widely used in cancer histopathology but its functions remain unclear. Here, we show that Ki-67 controls heterochromatin organisation. Altering Ki-67 expression levels did not significantly affect cell proliferation in vivo. Ki-67 mutant mice developed normally and cells lacking Ki-67 proliferated efficiently. Conversely, upregulation of Ki-67 expression in differentiated tissues did not inhibit cell cycle arrest. Ki-67 interactors included proteins involved in nucleolar processes and chromatin regulators. Ki-67 depletion disrupted nucleologenesis but did not inhibit pre-rRNA processing. In contrast, it altered gene expression. Ki-67 silencing also had wide-ranging effects on chromatin organisation, disrupting heterochromatin compaction and long-range genomic interactions. Trimethylation of histone H3K9 and H4K20 at heterochromatin was strongly reduced. Overexpression of human or Xenopus Ki-67 induced ectopic heterochromatin formation. Altogether, our results suggest that Ki-67 expression in proliferating cells spatially organises heterochromatin, thereby controlling gene expression.

2018-10-26 | PXD003551 | Pride

Next Generation Sequencing Quantitative Analysis of Wild Type, CDK8-/-, CDK19-/-, and CDK8-/-CDK19-/- mouse instestinal organoids transcriptomes

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Global transcriptome profiling of Oct4/Klf4/Sox2 (3Factor, 3F) + IL6 iPS clones derived from mouse embryonic fibroblasts.

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