Data from: Dynamic NF-κB and E2F interactions control the priority and timing of inflammatory signalling and cell proliferation
Data files
May 04, 2017 version files 18.72 MB
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020611 ALL CELLS_SK-N-AS.xlsx
1.56 MB
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021009 061109 061109e combined.xls
999.42 KB
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090909 HeLa FUCCI r2 ANALYSIS.xls
1.52 MB
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120210 AS FUCCI O+G CTRL ANALYSIS.xls
2.26 MB
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BAC BAC Stable cell phase Meta data_Dryad.xls
2.32 MB
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C11_nuc_table.xlsx
210 KB
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C11_TNF.xlsx
2.70 MB
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Origin cc.opj
772.54 KB
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Representitive cell traces.xlsx
6.37 MB
Abstract
Dynamic cellular systems reprogram gene expression to ensure appropriate cellular fate responses to specific extracellular cues. Here we demonstrate that the dynamics of Nuclear Factor kappa B (NF-κB) signalling and the cell cycle are prioritised differently depending on the timing of an inflammatory signal. Using iterative experimental and computational analyses, we show physical and functional interactions between NF-κB and the E2 Factor 1 (E2F-1) and E2 Factor 4 (E2F-4) cell cycle regulators. These interactions modulate the NF-κB response. In S-phase, the NF-κB response was delayed or repressed, while cell cycle progression was unimpeded. By contrast, activation of NF-κB at the G1/S boundary resulted in a longer cell cycle and more synchronous initial NF-κB responses between cells. These data identify new mechanisms by which the cellular response to stress is differentially controlled at different stages of the cell cycle.