In This Issue
People & Ideas
Biochemical, cytological, and lipidomic approaches show that lipid droplets are dispensable as membrane sources for autophagy, but are required for ER homeostasis by buffering fatty acid synthesis and ER stress and maintaining phospholipid composition to allow autophagy regulation and autophagosome biogenesis.
Strategies to regulate transcription factor–mediated gene positioning and interchromosomal clustering at the nuclear periphery
In yeast, transcription factors mediate gene positioning at the nuclear periphery and interchromosomal clustering. These phenomena are regulated by several different strategies that lead to dynamic changes in the spatial arrangement of genes over different time scales.
The spindle assembly checkpoint (SAC) ensures genome stability during cell division. Here, a new essential SAC factor, ARHGEF17, is characterized by quantitative imaging, biochemical, and biophysical experiments, which show that it targets the checkpoint kinase Mps1 to kinetochores.
Drosophila Arl2 governs neuroblast asymmetric cell division through regulation of microtubule growth and localization of Msps to centrosomes.
Analysis of luminal lysosomal pH in combination with heterologous expression of lysosomal-associated proteins indicates that peripheral lysosomes are more alkaline than juxtanuclear ones and that depletion of Rab7 and its effector, RILP, are associated with and can account for the reduced acidification.
β3 integrin–mediated spreading induced by matrix-bound BMP-2 controls Smad signaling in a stiffness-independent manner
Matrix-bound BMP-2 is sufficient to induce β3 integrin–dependent, Cdc42/Src/FAK/ILK-mediated cell spreading by overriding the stiffness response through actin and adhesion site dynamics, showing BMP receptors and integrins work together to control signaling and tensional homeostasis, thereby coupling cell adhesion and fate commitment.
Loss of miR-203 regulates cell shape and matrix adhesion through ROBO1/Rac/FAK in response to stiffness
Increased stiffness in the tumor microenvironment generates forces on cells that promote cancer development. A signaling circuit is identified through which cells sense and respond to these changes. Patients whose tumors express these genes exhibit a better overall survival prognosis.
Collagen-derived matricryptins promote inhibitory nerve terminal formation in the developing neocortex
A proteolytically released fragment of collagen XIX, termed a matricryptin, promotes the assembly of inhibitory nerve terminals through integrin receptors.