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The ciliary transition zone (TZ) at the base of cilia is thought to gate entry of proteins into the cilium. The authors characterize a role for TMEM107, a protein mutated in the ciliopathy Joubert syndrome, in organizing a submodule of the TZ.
Baskin et al. report that FAM126A, which is mutated in hypomyelination and congenital cataract, regulates PI4KIII, the kinase generating PtdIns(4)P. Loss of FAM126A in patients affects PI4KIIIα complex assembly and PtdIns(4)P synthesis at the plasma membrane.
Samakovlis and colleagues perform a genome-wide, tissue-specific RNAi screen in the Drosophila larval and adult airway systems and find that an initial transient anisotropic distribution of aPKC drives fibre orientation during tube formation.
Using live imaging, St Johnston and colleagues show in three Drosophila epithelia that cells born outside the epithelium do not die, but reintegrate, and that lateral adhesion is required for reintegration to occur.
Through a proteomic analysis of ER–PM junctions, Zhou and colleagues and Wang and colleagues discover that the transmembrane protein STIMATE is a positive regulator of STIM localization and function, thereby stimulating Ca2+ influx.
Lu and colleagues report that the O-GlcNAcylated MIF cytokine binds the extracellular domain of EGFR and prevents EGF-induced EGFR activation. Conversely, EGFR activation leads to MMP13-mediated MIF degradation and EGFR-induced tumorigenesis
Lehmann and colleagues describe a role for the ATP synthase in Drosophila germline stem cell differentiation that is independent of ATP synthesis, and involves the maturation of mitochondrial cristae.
Using C. elegans zygotes, Dumont and colleagues find that kinetochore proteins, including KNL-1, participate in assembly of central spindle microtubules for cytokinesis.
Bergert et al. use theoretical modelling and cell-based experiments to show that adhesion-independent cell migration is powered by nonspecific substrate friction, with smaller forces exerted compared with those of focal-adhesion-dependent movement.
Castanon, González-Gaitán and colleagues report that Sara endosomes can regulate asymmetric cell division by unequally positioning endocytosed Notch ligand in one daughter cell.