This week’s articles showed that enhancing a mitochondrial stress response reduced amyloid aggregation in mice; solved the structure of the ion channel TRPM4; found a role for NOTCH1 in the assembly of adherens junctions and endothelial barrier maintenance; and showed that RNA polymerase III limits life span in worms and flies.
ALZHEIMER’S DISEASE
Mitochondrial proteostasis and amyloid aggregation
Sorrentino et al. found that enhancing mitochondrial proteostasis reduced amyloid aggregation in mouse models of Alzheimer’s diease.
STRUCTURAL BIOLOGY
Revealing the architecture of TRPM4
Winkler et al. and Guo et al. used cryo–electron microscopy to solve the structure of the calcium-activated, nonselective ion channel TRPM4, providing insights into its function and pharmacology.
MECHANOTRANSDUCTION
Linking transcription programs with adhesion
Polacheck et al. showed that shear stress stimulates the formation of a NOTCH1-containing complex that stimulates adherens junction formation and the maintenance of endothelial barrier function.
AGING
Targeting RNA polymerase III to combat aging?
Filer et al. found that RNA polymerase III limits life span in worms and flies downstream of the kinase complex TORC1 (see also Edgar and Grewal).
