Bowman et al. show that in melanocytes, the vSNARE VAMP7 is sorted from endosomes into tubular membrane transport carriers bound for maturing melanosomes in a complex with the tSNARE syntaxin 13 via redundant recognition of each SNARE by an AP-3–BLOC-1 super-complex.

Centromeric transcription is critical for proper centromere function, but its exact role remains elusive. By manipulating the activity of centromeric transcription, Chen et al. report that a major function of centromeric transcription in human cells is to maintain centromeric cohesion.

Nthiga et al. identify CALCOCO1 as a receptor for autophagic degradation of Golgi during nutrient starvation. CALCOCO1 binds the Golgi-resident palmitoyltransferase ZDHHC17 and ATG8 family proteins to facilitate Golgiphagy to control Golgi size. Depletion of CALCOCO1 causes expansion of the Golgi and accumulation of its structural and membrane proteins.

How lipid droplets are formed is largely unclear. Chen et al. show that FIT2 recruits ER tubule-forming proteins and septin cytoskeletons to facilitate nascent LD formation by providing membrane curvature and bulging scaffold.

May et al. combine proximity labeling with quantitative mass spectrometry to profile the proteome of primary cilia in cells responding to Hedgehog. They identify signaling factors that undergo dynamic ciliary enrichment and uncover an unanticipated regulation of ciliary cAMP signaling.

Doodhi et al. reconstitute the yeast kinetochore–microtubule interface in vitro and compare the relative strength of distinct kinetochore–microtubule interaction modes. Their results suggest how Aurora B kinase promotes the exchange of kinetochore–microtubule interactions to eliminate aberrant interactions and establish chromosome biorientation.

Vessoni et al. demonstrate telomere shortening leads to a unique DDR response in human pluripotent stem cells. Unlike terminally differentiated cells, telomere shortening induces formation of single-stranded DNA telomere overhangs in hPSCs, which activate ATR signaling and lead to mitotic catastrophe and p53-dependent cell death.