- 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.
- How TPX2 promotes branching microtubule nucleation
TPX2 is required for microtubule nucleation in mitosis, but the mechanism underlying its function is unclear. Alfaro-Aco et al. analyze the domains of TPX2 necessary for its activity and identify the minimal region required for branching microtubule nucleation.
- Spectral shifts of acridine orange with CNS injury
Plemel et al. use a spectrally sensitive nucleic acid dye, acridine orange, to demonstrate a loss of RNA early during cell death. Acridine orange can also be used to distinguish apoptosis from necrosis/necroptosis in vitro and in fixed tissue samples.
- Role of eIF2α in dendritic degeneration
Xin Qi previews work by Tsuyama and colleagues linking eIF2α phosphorylation-mediated control of translation with neuronal subtype-specific mitochondrial stress-induced dendritic branching defects.
- Competitive control of end resection by TOPBP1
Shimada and Gasser discuss new findings from the Smolka laboratory supporting a competitive model for nonhomologous end joining and homologous recombination factors at DNA breaks.
- CLUH regulates transcripts of metabolic enzymes
CLUH binds mRNAs implicated in intermediate metabolism and oxidative phosphorylation, but the physiological and molecular significance of these interactions is unclear. Schatton et al. use new constitutive and liver-specific Cluh knockouts to define the function of CLUH in catabolic and energy-converting pathways as a regulator of the translation and stability of target mRNAs.
- VHL–NF-κB regulate VCAM-1 in ccRCC cells
Labrousse-Arias et al. show that VHL expression leads to increased VCAM-1 levels in renal cell carcinoma through an NF-κB–dependent mechanism that seems to contribute to the antitumoral immune response. This study also suggests that VCAM-1 levels might serve as a marker of ccRCC progression in human patients.
- VDAC2–BAK axis permeabilizes peroxisome membrane
VDAC2 controls the stable localization of BAK to mitochondria and its ability to mediate mitochondrial outer membrane permeabilization. Hosoi et al. now report that BAK shifts from mitochondria to peroxisomes under VDAC2-deficient conditions, giving rise to the mislocalization of peroxisomal matrix proteins such as catalase, which suggests that BAK can also regulate the permeability of peroxisomal membranes.