Chan et al. show that natural killer (NK) cells can be reprogrammed by breast cancer cells to promote metastasis. Reprogramming can be blocked by targeting NK cell inhibitory receptors TIGIT or KLRG1 or inhibiting DNA methyltransferases, which suggests new approaches to prevent or treat metastasis.

Chen et al. identified a bipartite motif from the 440-kD giant ankyrin-B, which bundles and avidly binds to microtubules in vitro. They further demonstrated that giant ankyrin-B suppresses axon collateral branching and prevents microtubule invasion of nascent axon branches through direct interaction with microtubules.

A single alternatively spliced exon in the CLTC gene contributes to clathrin coat organization. This event participates in the plasticity from clathrin-coated pits to plaques, structures that are essential for muscle fiber function and maintenance.

Jiang and colleagues investigate how locations of sites of organelle assembly are determined during cell division in the ciliate Tetrahymena thermophila. They find that correct placement of new organelles involves antagonistic influences of a cyclin E and a Hippo/Mst kinase.

CDKA;1, the Arabidopsis orthologue of Cdk1 and Cdk2, controls microtubule organization in meiosis. Sofroni et al. find that reducing CDKA;1 activity converts simultaneous cytokinesis—the separation of all four meiotic products concomitantly—into two successive cytokineses after the first and second meiotic divisions, as found in many crop species.

Begovich et al. identify 17 metabolic enzymes that are stress-specific components of yeast stress granules (SGs). The product of one of these enzymes, AdoMet, is an evolutionarily conserved regulator of SG assembly and blocks the recruitment of pathogenic TDP-43 into SGs in ALS models, highlighting its therapeutic potential.

Ko et al. demonstrate that SARM1 is required for loss of axons and neurons in a neuroinflammatory model of glaucoma. Neuroinflammatory signaling induces an axonal necroptosis that triggers SARM1-dependent axon degeneration. These findings delineate unexpected molecular and functional relationships among neuroinflammation, necroptosis, and axon degeneration.