DNA concentration, cyclin levels, phosphatase activity, and CDK phosphorylation combine to directly link cell size to cell division.

An evolutionary algorithm is used to build gene networks implementing cell size control, and suggests multiple ways for evolution to first build sizers and turn them into adders depending on evolutionary constraints.

Yeast cell size homeostasis is not controlled by a G1-specific mechanism alone but is likely to be an emergent property resulting from the integration of several mechanisms that coordinate cell and bud growth with division.

Vacuolar morphologenesis correlates with cell size and is required for auxin-dependent inhibition of growth.

The p38 MAPK pathway functions downstream of a cell-size-sensing process to coordinate cell size/growth with G1 progression in animal cells.

It is shown that fission yeast cells sense their size by measuring their surface area through a membrane-associated sizer protein cdr2p.

Advanced microscopy techniques reveal that clusters of Pom1 kinase at the membrane represent the functional unit that shape the concentration gradients and modulate Pom1 mid-cell levels according to cell size.

CDKG1 is a D-cyclin dependent retinoblastoma related protein kinase whose abundance scales with cell size and controls cell division cycle number during multiple fission.

Cells employ two strategies, adjusting both their cell cycle lengths and their growth rates in a size-dependent manner, to correct aberrations in cell size.

Analysis of experiments on bacteria suggests that the dependence of cell size on growth rate is not an adaptation but a causal consequence of a regulatory mechanism that controls DNA replication.