A sudden fall in the levels of the coenzyme NADPH within cells could have a central role in the process of aging.

Sphingolipids govern the compartmentalization of yeast cells through the assembly of lateral diffusion barriers in ER membranes.

Protons are pumped out of mother cells by a protein that accumulates over time and this leads to cellular aging, but this protein is largely absent from daughter cells, which mediates rejuvenation.

The SAGA complex binds non-chromosomal DNA circles and prevents their spreading by attaching them to nuclear pores, thereby leading to the concomitant accumulation of DNA circles and pores in ageing yeast mother cells.

Cell division imposes a limit on proteostasis capacity by reducing chaperone accumulation, but chaperone-substrate interactions reverse these events to allow clearance of even chronically misfolded protein amyloids.

A mathematical model that combines stochasticity and spatial structure describes the dynamics of the viral population during an infection cycle, and fitting the model to RNA and virus abundances over time shows that poliovirus follows a geometric replication mode.

Senescent cells are recurrently induced during limb regeneration in salamanders and subsequently eliminated by a highly efficient mechanism of macrophage-dependent surveillance.

Endoplasmic reticulum (ER) inheritance regulation during ER stress controls the transmission of misfolded ER proteins from mother to daughter cell in budding yeast.

CaMKI and neuroendocrine signaling integrate information about food status to regulate a developmental decision in C. elegans.

Expression of the lamina-associated polypeptide α (LAP2α) prevents premature cellular ageing caused by expression of progerin in Hutchinson-Gilford progeria syndrome.