Applying dynamical systems theory to single-cell data can provide a detailed picture of the cellular states observed during cell fate decisions. This study presents a dynamic landscape analysis (DLA) ...

Cells are the building blocks of biological complexity. They are complex systems sustained by the coordinated cooperative dynamics of several biochemical networks. Their replication, adaptation and co...

Kale et al. show that nuclear divisions are defective at elevated temperature, leading to gastrulation defects and embryo lethality. Their work finds that F-actin – microtubule interactions during mit...

Complex multicellularity has evolved in just five lineages (animals, plants, brown algae, red algae, and fungi) and in each case, these organisms develop clonally and are obligately multicellular. While prior work has shown that clonal development plays a critical role in the evolution of complex multicellularity, none has disentangled this from the impact of obligate vs facultative multicellular life cycles. Here we use experimental evolution with engineered snowflake yeast ( Saccharomyces cerevisiae ) to directly test how life cycle structure affects multicellular adaptation. We created isogenic strains capable of switching between unicellular and clonal multicellular phases, then evolved populations for 192 days under obligately multicellular, facultatively multicellular, and obligately unicellular regimes. Obligately multicellular populations rapidly evolved larger size, primarily driven by a whole genome duplication, in all five replicates. Facultative populations showed dramatically constrained evolution, with tetraploidy evolving in only 2/10 facultative populations despite experiments demonstrating that it is strongly beneficial across the full life cycle. Mathematical modeling reveals the mechanistic basis for this constraint: facultative life cycles create establishment barriers through two population genetic effects. Group formation dramatically reduces the number of units of selection, making beneficial multicellular mutations vulnerable to drift. This asymmetry in population size between life cycle phases also allows cell-level selection to overpower group-level selection, eliminating mutations that provide group-level benefits but carry cell-level costs. These findings demonstrate that obligate multicellularity circumvents fundamental population genetic barriers to collective-level adaptation, helping explain why complex multicellularity has evolved exclusively in obligately multicellular lineages, and suggesting similar constraints may operate in other evolutionary transitions in individuality. ### Competing Interest Statement The authors have declared no competing interest. U.S. National Science Foundation, https://ror.org/021nxhr62, DEB-1845363 Howard Hughes Medical Institute Gilliam Fellowship National Science Foundation Graduate Research Fellowship

Autorino et al. report a feedback loop between Nodal signalling and tissue phase transitions in zebrafish embryos. Nodal alters adhesion, triggering tissue rigidification and reduced porosity, which l...

On AI agents, grunt work, and the part of science that isn't replaceable.

For many of us who work in scientific publishing, the title of this Editorial is a question we hear all the time when we're out talking to academics. And it's a perfectly reasonable one. After all, re...

Cells use fluid flow to deliver proteins to their leading edge. An actin barrier creates a compartment where contraction drives flow, steering proteins toward growing regions. This mechanism coordinat...

Nature Reviews Genetics - In this Perspective, Maizels and Briscoe discuss the limitations of current models of gene regulatory networks and outline solutions to harness data abundance without...

Intracellular transport of macromolecules is crucial for the proper functioning of most cellular processes. Although intracellular crowding is know...

The cytoskeleton, a dynamic and intricate network of protein filaments, is found within the cytoplasm of all cells, from bacteria and archaea to complex eukaryotes. This essential cellular component …

Scientists have identified tubulin structures in primitive Asgard archea that may have been the precursor of our own cellular skeletons.

Self-organized criticality can occur in cellular systems, but its origins remain unclear. Now it is shown that cytoskeletal criticality is influenced by the F-actin architecture and myosin active stre...

Understanding of the dynamics inherent to biological matter is crucial for illuminating the physical mechanisms underlying cellular processes. In this study, we employ bright-field differential dynamic microscopy (DDM) to investigate density fluctuations inherent in a cell-free model of eukaryotic cytoplasm. Our measurements reveal subdiffusive fractional Brownian motion and non-Gaussian displacement distributions, highlighting cytoplasmic heterogeneity. We introduce an empirical model that combines fractional Brownian motion with an inverse Gaussian distribution of diffusivities to describe the observed non-Gaussianity. Validated through Monte Carlo simulations, this model allows us to estimate the fractional diffusivity and exponent effectively. By altering macromolecular composition, the addition of energy, and assembly of a cytoskeleton, we identify three independent mechanisms that result in similar fractional exponents yet distinct diffusivities. We find that energy addition leads to non-stationary dynamics, in contrast to the stationary behavior observed under passive conditions. Presence of microtubules introduces a secondary dynamical timescale, which we describe using a two-state fractional Brownian motion model to differentiate between cytosolic and microtubule network associated contributions. Our findings demonstrate the effectiveness of DDM as a label-free tool for quantifying viscoelastic and heterogeneous properties of the cytoplasm and provide insights into how physical and biochemical factors, including cytoskeletal organization, govern subcellular dynamics. ### Competing Interest Statement The authors have declared no competing interest.

President Trump’s immigration crackdown ensnared Kseniia Petrova, a scientist who fled Russia after protesting its invasion of Ukraine. She fears arrest if she is deported there.