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.

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.

Dosage-compensated gene expression facilitates chromosomal aneuploidy, which presents a rapid route to phenotypic evolution in natural yeast isolates.

Increased catalysis has been suggested to be an adaptive trait of enzymes to growth at lower temperature, but systematic analysis suggests that temperature exerts a weak selection pressure on enzyme rate enhancement, with observed variation arising from other evolutionary forces.

IL-6 gene and protein expression are rapidly and transiently upregulated in the choroid in response to myopic defocus, as a result of prior form deprivation or treatment with +15 D lenses in a nitric oxide-dependent manner.

Mutations elsewhere in the genome play critical roles in improving fitness during amplification and divergence of a gene encoding a weak-link enzyme whose inefficiency limits growth rate.

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.

By properly accounting for gene copy number and cell-cycle effects, single cell snapshots of nascent and mature mRNA can be used to unveil the stochastic kinetics of gene activity.

Transmissible tumors in Hydra can manipulate host phenotype by inducing the growth of supernumerary tentacles, enhancing host foraging efficiency and promoting tumor vertical transmission, akin to manipulative parasites.

The genetic make-up of dominating MDR-TB clades in Central Asia is shaped by programmatic and socio-economic changes that led to fixation of resistance and bacterial fitness related mutations in the Soviet era.