Zewe et al. develop approaches to map the subcellular distribution of the major phospholipid, phosphatidylinositol (PI), revealing that the lipid is present in most membranes except for plasma membrane, where it is found mainly as PI4P and PI(4,5)P2.

Itakura et al. identify a protein quality control system for aberrant extracellular proteins, including misfolded proteins and amyloid β. This extracellular proteostasis pathway involves the cell-surface heparan sulfate receptor, which mediates internalization of aberrant extracellular proteins in complex with an extracellular chaperone.

Pemberton et al. characterize a molecular toolbox for the visualization and manipulation of phosphatidylinositol (PI) within intact cells. Results using these approaches define the steady-state distribution of PI across subcellular membrane compartments and provide new insights into the relationship between PI availability and polyphosphoinositide turnover.

Viol et al. show that the conserved Never-in-mitosis-A–related kinase-2 (Nek2) removes distal appendage components from the mother centriole prior to mitosis in every cell cycle. These findings suggest that Nek2 prevents cilia maintenance during mitosis via distal appendage regulation.

Cairo et al. show that in S. cerevisiae meiosis, spindle checkpoint proteins Bub1 and Bub3 have a critical role in preventing chromosome missegregation and setting the normal duration of anaphase I and II onset by regulating the kinetochore-localization of Ipl1 and PP1.

ALIX recruits ESCRT-III onto endosomes in a process that does not depend on other ESCRTs but requires the late endosome–specific lipid LBPA in vivo and in vitro. This novel pathway of ILV formation promotes tetraspanin sorting and delivery to exosomes.

Centrosomes withstand microtubule-mediated forces during spindle assembly, yet they are disassembled by similar forces during mitotic exit. Mittasch et al. use nanorheology to probe the material properties of centrosomes and how they change during the cell cycle. In anaphase, the centrosome scaffold becomes weak and brittle, thus allowing force-induced disassembly.