For some size control networks, cell size consistently decreases in each cycle until a burst of cell cycle inhibitor drives an extended G1 phase much like the cell division cycle of the green algae Chlamydomonas. Sizers also evolve when the cell cycle structure is inverted so that G1 is a timer, while S/G2/M performs size control, as is the case for the fission yeast S. But, if the G1 phase is significantly longer than the S/G2/M phase, as is often the case in mammalian cells in vivo, sizers become more likely. If the mechanism is based on a G1 size control and an S/G2/M timer, as found for budding yeast and some human cells, adders likely evolve. Moreover, evolved networks recapitulated known size control properties of naturally occurring networks. The size control mechanism that evolved was influenced by both cell cycle structure and specific selection pressures.
#SCHEMATIC UNSTABLE TEMPORAL TIME SHIFTER RANK3 DROP CHANCE SERIES#
This diversity raises the question why a particular cell would implement one rather than another mechanism? To address this question, we performed a series of simulations evolving cell size control networks. To control their size, cells use diverse mechanisms ranging from ‘sizers’, in which differences in cell size are compensated for in a single cell division cycle, to ‘adders’, in which a constant amount of cell growth occurs in each cell cycle. Cell size is controlled to be within a specific range to support physiological function.
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