Parental B-MYB/FOXM1 controls mitotic E2F to determine daughter cell fate
Mitogens trigger cell-cycle entry by activating E2F at the restriction point, which is followed by B-MYB/FOXM1 activation and progression to mitosis. How mitogens control continued cycling and cell-cycle exit after the restriction point is not well-understood. By developing an E2F and B-MYB/FOXM1 dual transcriptional biosensor system, we show that S/G2 phase duration is set by timed…
Parental B-MYB/FOXM1 activation controls mitotic E2F levels to determine whether a cell continues cycling or exits the cell cycle after the restriction point, according to a new study. Researchers have developed a dual transcriptional biosensor system to investigate how mitogens regulate the timing of B-MYB/FOXM1 activation and its impact on cell-cycle progression.
Their findings reveal that S/G2 phase duration is determined by the precise timing of B-MYB/FOXM1 activation, while E2F activity gradually diminishes before mitosis. Rapid B-MYB/FOXM1 activation leads to shorter S/G2 phases and high mitotic E2F activity in daughter cells, keeping them cycling. Conversely, delayed B-MYB/FOXM1 activation results in longer S/G2 phases, reducing mitotic E2F levels and driving daughter cells into quiescence.
If S/G2 remains prolonged, partially activated B-MYB/FOXM1 can revert, triggering mitotic bypass and potentially leading to polyploid quiescence. In summary, B-MYB/FOXM1 plays a critical role in governing cell fate by establishing a tri-directional control mechanism at the G2 restriction point.
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