Arbovirus impact on mosquito behavior: the jury is still out.

Parasites can manipulate host behavior to enhance transmission, but our understanding of arbovirus-induced changes in mosquito behavior is limited. Here, we explore current knowledge on such behavioral alterations in mosquito vectors, focusing on host-seeking and blood-feeding behaviors. Reviewing studies on dengue, Zika, La Crosse, Sindbis, and West Nile viruses in Aedes or Culex mosquitoes reveals subtle yet potentially significant effects. However, assay heterogeneity and limited sample sizes challenge definitive conclusions. To enhance robustness, we propose using deep-learning tools for automated behavior quantification and stress the need for standardized assays. Additionally, conducting longitudinal studies across the extrinsic incubation period and integrating diverse traits into modeling frameworks are crucial for understanding the nuanced implications of arbovirus-induced behavioral changes for virus transmission dynamics.

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. Gene-expression speed constrains cells' ROS-reducing rate and sets the shortest possible doubling-time. To replicate, cells require below-threshold concentrations of ROS. Thus, cells with sufficiently abundant ROS remain in G1, become unsustainably large and, consequently, burst. Therefore, at a given temperature, yeast's replicative life cannot progress arbitrarily slowly and cells with the lowest ROS-levels replicate most rapidly. Fundamental barriers may constrain the thermal slowing of other organisms' lives.

Dormancy-to-death transition in yeast spores occurs due to gradual loss of gene-expressing ability.

Dormancy is colloquially considered as extending lifespan by being still. Starved yeasts form dormant spores that wake-up (germinate) when nutrients reappear but cannot germinate (die) after some time. What sets their lifespans and how they age are open questions because what processes occur-and by how much-within each dormant spore remains unclear. With single-cell-level measurements, we discovered how dormant yeast spores age and die: spores have a quantifiable gene-expressing ability during dormancy that decreases over days to months until it vanishes, causing death. Specifically, each spore has a different probability of germinating that decreases because its ability to-without nutrients-express genes decreases, as revealed by a synthetic circuit that forces GFP expression during dormancy. Decreasing amounts of molecules required for gene expression-including RNA polymerases-decreases gene-expressing ability which then decreases chances of germinating. Spores gradually lose these molecules because they are produced too slowly compared with their degradations, causing gene-expressing ability to eventually vanish and, thus, death. Our work provides a systems-level view of dormancy-to-death transition.

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).

A collective path toward regeneration.

How do cells collectively control an organ's behavior? By plucking various numbers of hairs from the mouse skin, Chen et al. show that hairs regenerate only when a sufficiently high density of them are plucked. Remarkably, a hair follicle can only regenerate in concert with other follicles, but not autonomously.

Molecular-Level Tuning of Cellular Autonomy Controls the Collective Behaviors of Cell Populations.

A rigorous understanding of how multicellular behaviors arise from the actions of single cells requires quantitative frameworks that bridge the gap between genetic circuits, the arrangement of cells in space, and population-level behaviors. Here, we provide such a framework for a ubiquitous class of multicellular systems-namely, "secrete-and-sense cells" that communicate by secreting and sensing a signaling molecule. By using formal, mathematical arguments and introducing the concept of a phenotype diagram, we show how these cells tune their degrees of autonomous and collective behavior to realize distinct single-cell and population-level phenotypes; these phenomena have biological analogs, such as quorum sensing or paracrine signaling. We also define the "entropy of population," a measurement of the number of arrangements that a population of cells can assume, and demonstrate how a decrease in the entropy of population accompanies the formation of ordered spatial patterns. Our conceptual framework ties together diverse systems, including tissues and microbes, with common principles.