Data from: Dynamic NF-κB and E2F interactions control the priority and timing of inflammatory signalling and cell proliferation

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.