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
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021009 061109 061109e combined.xls
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090909 HeLa FUCCI r2 ANALYSIS.xls
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120210 AS FUCCI O+G CTRL ANALYSIS.xls
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BAC BAC Stable cell phase Meta data_Dryad.xls
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C11_nuc_table.xlsx
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C11_TNF.xlsx
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Origin cc.opj
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Representitive cell traces.xlsx
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.