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pmid:26697349

Transcriptomic profiling of human embryonic stem cells upon cell cycle manipulation during pluripotent state dissolution.

Kevin Andrew Uy Gonzales · Hongqing Liang

Genomics data · 2015 doi:10.1016/j.gdata.2015.08.032

Paper

complete

Experiment

complete

Data

partial

Analysis

partial

Execution

absent

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Transcriptomic profiling of human embryonic stem cells upon cell cycle manipulation during pluripotent state dissolution.
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10.1016/j.gdata.2015.08.032
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Kevin Andrew Uy Gonzales
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Hongqing Liang
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Genomics data
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2015
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While distinct cell cycle structures have been known to correlate with pluripotent or differentiated cell states [1], there is no evidence on how the cell cycle machinery directly contributes to human embryonic stem cell (hESC) pluripotency. We established a determinant role of cell cycle machineries on the pluripotent state by demonstrating that the specific perturbation of the S and G2 phases can prevent pluripotent state dissolution (PSD) [2]. Active mechanisms in these phases, such as the DNA damage checkpoint and Cyclin B1, promote the pluripotent state [2]. To understand the mechanisms behind the effect on PSD by these pathways in hESCs, we performed comprehensive gene expression analysis by time-course microarray experiments. From these datasets, we observed expression changes in genes involved in the TGFβ signaling pathway, which has a well-established role in hESC maintenance [3], [4], [5]. The microarray data have been deposited in NCBI's Gene Expression Omnibus (GEO) and can be accessed through GEO Series accession numbers GSE62062 and GSE63215.
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Differentially expressed genes were obtained using the Significance Analysis of Microarrays software (http://statweb.stanford.edu/~tibs/SAM/) and gene ontology analysis was done using DAVID (https://david.ncifcrf.gov/).
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An RNAi screen probing signalling control of human embryonic stem cells establishes the cell cycle-regulated restriction of the exit from pluripotency (DNA damage checkpoint)
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