In Drosophila melanogaster, nutrition controls body size by acting through the Forkhead Box class O (FoxO)/Ultraspiracle complex to regulate nutrition-sensitive ecdysone biosynthesis, thereby controlling the switch to stop growth.

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.

The cell junction-associated protein Amotl2a controls tissue size in the zebrafish lateral line primordium by limiting the activity of the Hippo effector Yap1 and the Wnt effector Lef1.

Size regulation of the otic vesicle, the progenitor of the inner ear, is mediated by mechanical feedback involving fluid influx, hydraulic pressure, and tissue mechanics.

Signaling from the limb nerves regulates the rate of growth and the overall size of the regenerating limb.

The volume of the nucleus is dictated by a balance of colloid osmotic forces from the nucleoplasm and cytoplasm.

The size of a subcellular structure, yeast actin cables, scales with the linear dimensions of the cell, which is achieved by feedback control of their growth rate.

JNK signaling is active in developing Drosophila tissues and is required for achieving proper organ size.

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.