Slowest possible replicative life at frigid temperatures for yeast.

Determining whether life can progress arbitrarily slowly may reveal fundamental barriers to staying out of thermal equilibrium for living systems. By monitoring budding yeast's slowed-down life at frigid temperatures and with modeling, we establish that Reactive Oxygen Species (ROS) and a global gene-expression speed quantitatively determine yeast's pace of life and impose temperature-dependent speed limits - shortest and longest possible cell-doubling times. Increasing cells' ROS concentration increases their doubling time by elongating the cell-growth (G1-phase) duration that precedes the cell-replication (S-G2-M) phase.

Yeasts collectively extend the limits of habitable temperatures by secreting glutathione.

The conventional view is that high temperatures cause microorganisms to replicate slowly or die. In this view, microorganisms autonomously combat heat-induced damages. However, microorganisms co-exist with each other, which raises the underexplored and timely question of whether microorganisms can cooperatively combat heat-induced damages at high temperatures.

Evaluation of Schink et al.: Having the Gem Shine through a Fog.

One snapshot of the peer review process for "Death Rate of E. coli during Starvation Is Set by Maintenance Cost and Biomass Recycling" (Schink et al., 2019).

DNA origami scaffold for studying intrinsically disordered proteins of the nuclear pore complex.

The nuclear pore complex (NPC) is the gatekeeper for nuclear transport in eukaryotic cells. A key component of the NPC is the central shaft lined with intrinsically disordered proteins (IDPs) known as FG-Nups, which control the selective molecular traffic. Here, we present an approach to realize artificial NPC mimics that allows controlling the type and copy number of FG-Nups.