An iterative self-assembling algorithm identifies the intrinsic structures in single-cell transcriptomic data and helps to discover new cell populations that are undetectable by existing methods.

Harmful genetic variants at mendelian disease genes slow down adaptation, by interfering with the spread of adaptive variants in a population.

The damage of the bacterial cell envelope is found to be only a secondary effect of the antimicrobial activity of lactoferricin derivatives.

Selection for undifferentiated multicellularity emerges in an evolutionary cell-based model because a collective of cells performs chemotaxis better than single cells in a noisy environment.

Epigenomic and transcriptomic analysis reveals that paternal obesity influences sperm histone H3 lysine 4 tri-methylation enrichment and placenta gene expression, which in turn negatively impact its development and function in a manner that may contribute to metabolic disease in offspring.

Tracking of all cells in intestinal organoids crypts to fully reconstruct cell lineages reveals that proliferative behavior is highly symmetric between sisters cells, while simulations show that this observed symmetry minimizes random fluctuations in cell proliferation, thereby ensuring homeostasis.

Proteasomes are protected from autophagic elimination upon carbon starvation by sequestration into cytoplasmic storage granules, which aid cell fitness by providing a cache of proteasomes that can be rapidly remobilized when carbon availability improves.

Animal models reveal that mitochondrial complex I is dispensable for homeostatic functions of the mouse liver.

SARS-CoV-2 can spread efficiently within care homes causing outbreaks among residents, who are at increased risk of severe disease, emphasising the importance of stringent infection control in this population.