Issues

Two studies identify a signaling pathway that arrests cells that are having difficulty dividing.

Brangwynne’s work centers on the phase transitions that underlie various aspects of cell biology.

Grenfell et al. show that transcription and RNA processing occur in metaphase-arrested egg extracts and that noncoding RNA biogenesis is important for centromere, kinetochore, and mitotic spindle assembly.

Lambrus et al. show that centrosome loss or a prolonged mitosis activates a USP28–53BP1–p53–p21 signaling axis that prevents the growth of cells with an increased propensity for mitotic errors.

Meitinger et al. perform a genome-wide CRISPR/Cas9 screen for centrinone resistance and identify a 53BP1-USP28 module as critical for communicating mitotic challenges to the p53 circuit and TRIM37 as an enforcer of the singularity of centrosome assembly.

Tang et al. show that in fission yeast Myo51 is a single-headed class V myosin with two actin-binding sites: A typical ATP-dependent binding site and a novel ATP-independent site in its tail that requires binding partners Rng8/9. This molecular architecture allows Myo51 to slide actin-tropomyosin filaments relative to each other during contractile ring assembly.

G protein–coupled receptor CRHR1 activates both soluble adenylyl cyclase (sAC) and transmembrane adenylyl cyclases. Here, Inda et al. show that only sAC activity is essential for internalization-dependent cAMP and sustained ERK1/2 activation responses, revealing a functional association between sAC-generated cAMP and endosome-based G protein–coupled receptor signaling.

Sinha et al. show that the cytoskeletal and tumor-overexpressed protein cortactin promotes secretion of exosomes from cancer cells by stabilizing dynamic cortical actin docking sites for multivesicular endosomes, suggesting a potential mechanism by which cortactin may promote tumor aggressiveness.

Mammalian primordial germ cells proliferate while migrating, but the mechanisms regulating these opposing processes remain unclear. Here, Cantú et al. show that somatic cell microenvironments modulate germ cell proliferation via canonical Wnt signaling, whereas noncanonical Wnt5a–Ror2 signaling reciprocally promotes migration.