- Tensin and energy metabolism
Dornier and Norman discuss the findings by Georgiadou et al. that show that AMPK activity regulates tensin expression, thereby modulating α5β1-integrin and fibrillar adhesion assembly.
- Structure of the RZZ complex
The Rod–Zw10–Zwilch (RZZ) complex assembles as a fibrous corona on kinetochores before microtubule attachment during mitotic spindle formation. Mosalaganti et al. provide new structural insight into the Spindly–RZZ complex that suggests that it resembles a dynein adaptor–cargo pair in the kinetochore corona.
- Dynein recruitment to kinetochores
The dynein motor is recruited to the kinetochore to capture spindle microtubules and control the spindle assembly checkpoint. Gama et al. reveal the molecular mechanism of how the Rod–Zw10–Zwilch complex and Spindly mediate dynein recruitment in Caenorhabditis elegans and human cells.
- Role of INCENP domains in chromosome biorientation
The chromosomal passenger complex (CPC), which includes the Aurora B kinase and the scaffold Sli15/INCENP, promotes chromosome biorientation. Fink et al. engineer a minimal CPC construct made of Aurora B and Sli15/INCENP and determine how specific protein domains contribute to chromosome biorientation.
- 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.