Kif18a mutant mice produce micronuclei following segregation of unaligned chromosomes but do not spontaneously form tumors. KIF18A KO cells form stable micronuclear envelopes around lagging chromosomes located near the spindle pole and outside the midzone. These data suggest stable micronuclei may not actively promote tumorigenesis.

Ras GTPases are key membrane-associated elements of the EGFR-MAPK signaling pathway. Surve et al. demonstrate that endogenous KRAS and NRAS are predominantly localized to the plasma membrane and its tubular shaped protrusions and show that a small pool of surface EGFRs sustain signaling along the RAS-MAPK pathway, whereas internalized EGFRs do not significantly contribute to MAPK activity.

Chen et al. provide a novel insight on how poly(PR) dipeptides from C9orf72 gene exert cytotoxicity. The alternate distribution of Arg facilitates multivalent protein–protein interactions with proteins harboring acidic motifs and disturbs their functions through entrapment in the phase-separated droplets.

COPI vesicles recycle Golgi resident proteins within the Golgi stack. Welch et al. combine two orthogonal proteomic analyses to identify clients for the COPI adaptors GOLPH3 and GOLPH3L, and show that these adaptors interact with the cytoplasmic tails of enzymes from diverse glycosylation pathways by binding membrane-proximal positively charged residues.

Mitophagy is regulated by multiple interconnected pathways, which remain poorly understood in physiological settings. Shen et al. describe a mechanism of Pink1-dependent mitophagy utilizing Vps13D that acts in parallel to Parkin-mediated mitophagy during development.

This paper shows that adjacent cells with similar genetic capabilities to change their own shape enter a tug of war that determines which cell shrinks and which expands. For a cell to contract, its neighbors must yield, requiring a nonlinear stress–strain response in the mechanism governing its physical properties.

Isensee et al. describe a peripheral mechanism by which excitation of nociceptive sensory neurons leads to pain hypersensitivity. Depolarization of nociceptors results in cAMP-independent activation of type II protein kinase A (PKA-II) by calcium influx through CaV1.2 channels, which in turn modulates calcium channel activity.