Sánchez-Ramirez, Ung et al. show that NAD⁺ bioavailability controls adipogenic differentiation obstructing adipocyte commitment, downregulating ribosomal proteins–coding genes and leading to quiescent metabolic state. Instead, the NAD⁺-dependent SIRT1 deacetylase is essential for terminal differentiation of pre-adipocytes and regulates subcellular compartmentalization of redox metabolism during adipogenesis.

Hiragi et al. identify TBC1D18 as a Rab5-GAP that is associated with Mon1 and mediates endosome maturation. They propose a new endosome maturation model in which Mon1–Ccz1 together with TBC1D18 coordinates endosome maturation by inactivating Rab5 and activating Rab7.

Chromosome separation is coupled with cleavage furrow formation during anaphase. Sana, Rajeevan, et al. demonstrate that the mutually exclusive localization of NuMA and Ect2/Cyk4/Mklp1 ensures dynein/dynactin and RhoA at distinct membrane zones to coordinate chromosome separation with cleavage furrow formation.

Jia et al. identify cholesterol as the primary lipid responsible for interaction between Vibrio cholerae toxin MakA and host membranes. They further characterize a sophisticated mechanism of recurrent membrane damage regulated by pH-dependent pore formation, leading to V-ATPase-dependent unconventional LC3 lipidation on damaged endolysosomal membranes.

Liu et al. identify WDR91 as an important player in retromer-dependent recycling. WDR91 promotes the interaction of Rab7 with SNX-retromer components and interacts with FAM21, facilitating the formation of the endosomal retrieval subdomain.

Lysosomal damage induces stress granule (SG) formation and translational reprograming. The newly appreciated process of atg8ylation affects SG formation and concomitantly recruits SG core proteins NUFIP2 and G3BP1 to damaged lysosomes. These proteins independently of SG condensates and in coordination with galectin-8 inactivate mTOR via the Ragulator–Rag complex.

This work demonstrates the lipid composition and the corresponding biophysical properties of biological membranes to tune highly specific protein–lipid interactions. Specifically, cholesterol is shown to affect phosphoinositide-dependent membrane recruitment and translocation into the extracellular space of FGF2, a survival factor involved in tumor-induced angiogenesis.