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A wide range of bacterial species can switch into a cell wall-free state that does not require the FtsZ-based division machinery to proliferate.

Genome-scale metabolic modeling of individual cancer cells and healthy human cells identifies specific and selective metabolic vulnerabilities.

A new and general mechanism describes the organization of membrane proteins and their cytoplasmic ligands into micrometer-scale clusters, based on polymerization and concomitant phase separation of multivalent proteins.

Insights into the roles and mechanisms of two of the miRNAs upregulated in human breast cancer stem cells in at least some breast cancers are presented.

The SAGA complex binds non-chromosomal DNA circles and prevents their spreading by attaching them to nuclear pores, thereby leading to the concomitant accumulation of DNA circles and pores in ageing yeast mother cells.

Under insulinopenic conditions, the hormone adiponectin is essential for lipid uptake specifically in subcutaneous white adipose tissue, and is sufficient to ameliorate islet lipotoxicity.

In cell types that acquire planar cell polarity, the protein Flattop regulates basal body docking and positioning.

Endocytosis is triggered by membrane-associated proteins that transform the clathrin adaptor into an active complex.

TORC2-Ypk1 signaling upregulates flux through the sphingolipid pathway not only by increasing the supply of long-chain base precursors, but also by increasing their use in synthesizing complex sphingolipids.

The muniscin protein FCHO1 interacts with, and activates, the adapter protein-2 complex (AP-2) to promote the assembly of clathrin-coated vesicles.