About twenty temporal patterning genes are identified that drive an irreversible differentiation trajectory governing the heterogeneity and proliferative properties of cells in neural tumors with an early developmental origin.
A eukaryotic cell model overcomes metabolic deficiencies within a complex, self-establishing community that enables the growth-relevant exchange of metabolic intermediates.
Genetic and transcriptomic analyses revealed that eIF4E S209 phosphorylation enables Myc and mutant KRAS cooperation in colon cancer through stress- and glutamine-dependent growth and addiction.
Resting-state capillary blood flow and oxygenation are more homogeneous in the deeper cortical layers, underpinning an important mechanism by which the microvascular network adapts to an increased local oxidative metabolism.
Single-cell analysis of the chloroplast redox response to high light and oxidative stress revealed light-dependent heterogeneity, and was linked to cell fate determination within isogenic diatom populations.
Physiological differentiation during symbiosis leads to division of labor between smaller and larger cells in an uncultured bacterial tubeworm symbiont population and results in remarkable metabolic diversity and complexity.
Trypanosoma cruzi intracellular amastigotes exhibit rapid resistance to azoles, independent of genetic selection, which is dependent on metabolic state and mechanistically distinct from latency.
Mitochondrial dysfunction in neural stem cells and brain tumour cells decreases proliferation and affects the generation of neuronal diversity and tumour heterogeneity.
In a developing yeast colony, cells go from homogeneous states to spatially organized, specialized metabolic states, and the new metabolic states depend on resources produced by the original state.
Two novel subsets of microglia identified by their unique autofluorescence profiles differ in their subcellular organization, proteomic signatures and in their response to aging and lysosomal dysfunction.
