The combination of statistical inference and perturbation experiments reveals that trans-generational inheritance of cell size and cell-cycle speed, coupled through a minimum-size checkpoint, shapes paradoxical cell-cycle correlations in lineage trees.

Oversized mammalian cells reduce their growth efficiency by activating global protein degradation, which functions in parallel with the cell size checkpoints, to promote cell size homeostasis.

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

Cytoplasmic bodies sequester important abscission machinery to delay completion of cytokinesis in response to mitotic errors.

The S-phase checkpoint has roles in all phases of the cell cycle, which has implications for the majority of cancers that lack cell cycle controls.

Benzene mapping simulations of envelope protein rafts from six different flaviviruses reveal a conserved cryptic site whose cluster of ionisable residues is likely responsible for orchestrating pH-dependent conformational changes during fusion, thereby representing an attractive target for antiviral development.

ATR/Chk1 contribute to G2 arrest in developing tracheoblasts, and arrest in G2 facilitates cellular and hypertrophic organ growth.

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.

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.

Human cells center the position of the metaphase plate before anaphase onset to ensure the formation of equal-sized daughter cells.