This is achieved via the cell division cycle, which is driven by the sequential accumulation and destruction of cyclins.

Consistently, cells can be driven through the cell division cycle by artificial expression of a single CDK-cyclin fusion protein [43].

We propose here that bud size at division is a function of the growth rate in S-Gz-M, meaning that there is a common size control theme in the two growth phases of the cell division cycle.

In conclusion, we present a cell growth model, which unifies integration of growth and division in the G1 and G2 phases of the cell division cycle to accurately reproduce and predict cell size at birth and at budding, as well as timing of the cell cycle phases over four different nutritional conditions for budding yeast.

In the regulation of both the START and the Gz/M transitions, a master CDK is balanced against an opposing regulator that must be overcome to initiate crucial cellular events, like DNA replication or cell division [3].

Both in vivo and in silico analysis suggested that G1 is not the only size control phase during the cell division cycle [9, 10, 17, 32].

The idea that the surface area-to-volume-ratio plays an important role in connecting the cell growth to the cell division cycle was also eXplored by others [50, 57].

The higher noise at mitotic entry, inherent in Model-1, propagates directly to cell division ratios (Fig 4B), where cells that spend too much or little time in S-Gz-M produce abnormally large or small buds, respectively.