- Role of INCENP interactions in mitotic progression
The chromosomal passenger complex contributes to the activation of the mitotic checkpoint and is composed of INCENP, Survivin, Borealin, and the kinase Aurora B. Wheelock et al. define the role of the INCENP domains binding chromatin and microtubules in the mitotic checkpoint.
- FUS inclusions cause RNA mislocalization
Amyotrophic lateral sclerosis–associated mutations promote the formation of cytoplasmic FUS inclusions. In this study, Yasuda et al. show in fibroblasts and neurons that kinesin-1 is sequestered in FUS inclusions, resulting in a loss of detyrosinated microtubules and mislocalization of specific RNAs.
- Neurons eat glutamate to stay alive
Fendt and Verstreken preview work from Divakaruni et al. indicating that neurons can undergo metabolic changes to rely on glutamate for energy production, limiting excitotoxic injury.
- AMPK suppresses integrin activity through tensins
Georgiadou et al. show that the major metabolic sensor AMPK regulates integrin activity and integrin-dependent processes in fibroblasts by modulating tensin levels. Loss of AMPK up-regulates tensin expression, triggering enhanced integrin activity in fibrillar adhesions, fibronectin remodeling, and traction stress.
- Dynamics of FcγRI and SIRPα nanoclusters
Lopes et al. use superresolution microscopy to visualize the nanoscale organization of activating and inhibitory receptors on human macrophages. Nanoclusters of inhibitory SIRPα and activating FcγRI associate in the cell’s resting state, but engagement of FcγRI induces their segregation.
- Synapse-type specific recruitment of Munc13s
Munc13 proteins are key regulators of neurotransmitter release at presynaptic active zones. Kawabe et al. describe a molecular mechanism by which the active zone protein ELKS1 recruits a functionally unique Munc13 isoform, bMunc13-2, to a defined subset of synapses.
- Tango1 rings coordinate cargo exit from the ER
Drosophila melanogaster Tango1 is required for secretion of Collagen IV. Liu et al. use a genetic analysis to show that Tango1 is required to spatially maintain the size and integrity of ER exit site–Golgi units and that loss of Tango1 function impairs not only Collagen IV secretion but also general secretion.
- TANGO1 encircles COPII at ER exit sites
TANGO1 interacts with COPII components to generate a transport carrier for export of large cargo from the endoplasmic reticulum. Raote et al. show that TANGO1 molecules assemble to form a closed ribbon structure that encircles COPII components.