Qi et al. report a novel UHRF1 function as a nuclear protein catalyzing EG5 polyubiquitination for proper spindle architecture and faithful genomic transmission, which is independent of its roles in epigenetics and DNA damage repair. These findings reveal a previously unknown mechanism of UHRF1 controlling mitotic spindle architecture and chromosome behavior.

Tan et al. show that δ-catenin, previously thought to be neuron specific, is expressed by astrocytes and required both in astrocytes and neurons to control astrocyte morphogenesis. Furthermore, they provide evidence demonstrating how the cadherin–δ-catenin adhesion complex controls astrocyte morphology in a layer-specific manner.

Biton et al. elucidate how large secretory vesicles in Drosophila larval salivary glands employ a distinct machinery comprised of branched actin, myosin-II, and BAR-domain proteins to control fusion pore dynamics. This process facilitates a unique mode of exocytosis, which maintains apical membrane homeostasis during secretion.

Sullenberger et al. dissect the centrosomal patterning of Plk4 during centriole duplication and amplification and the positioning of Plk4 and procentrioles in relation to mother centriole microtubules. They build a molecular map of Cep57, Cep63, Cep192, and Cep152 and investigate their requirements for Plk4 localization.

Misfolded GPI-APs are released from the ER to the Golgi for rapid degradation in lysosomes by the constitutively active and stress-inducible RESET pathway. Using multiple complementary approaches, the authors demonstrate that competition by nascent glycoproteins for calnexin-binding promotes the release of misfolded GPI-APs for RESET.

Zhu et al. use Drosophila gentics and cell imaging to show that different types of γ-tubulin complexes can be recruited to mitotic centrosomes via different molecular pathways, that these centrosomes can nucleate microtubules even when they fail to recruit γ-tubulin, and that the dynamic properties of microtubules appear to be influenced by how they are nucleated.

During Drosophila border cell migration, the B-type lamin, Lam, maintains nuclear envelope integrity, stabilizes the lead cell protrusion, and promotes cluster invasion between nurse cells. The nucleus may function as a wedge to promote this collective, confined in vivo movement.