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    Le et al. demonstrate that a signaling pathway induced by SLIT2 and its receptor ROBO1 enhances focal adhesion formation when breast cells are subjected to stiff extracellular environments. SLIT2-treated normal murine mammary gland cells plated on fibronectin-coated glass substrates show robust focal adhesions containing activated FAK (red). The cells are also stained for F-actin (green) and DNA (blue).
    Image © 2016 Le et al.
    See page 707.

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ISSN 0021-9525
EISSN 1540-8140
In this Issue

In This Issue

In Focus

Lipid droplets regulate autophagy and cell survival by maintaining ER function in starving cells.

People & Ideas

Kadonaga studies the RNA polymerase II core promoter and chromatin assembly.



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.


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.

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.

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.

A proteolytically released fragment of collagen XIX, termed a matricryptin, promotes the assembly of inhibitory nerve terminals through integrin receptors.


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