Issues

The rapid swelling of yeast during hypoosmotic conditions is supported by the transport of the membrane and proteins from the ER to the cell surface. This transport seems to be mediated by the fusion of the cortical ER with the plasma membrane at membrane contact sites.

Mechanisms leading to abnormal distribution of neural progenitors during cortical development in the context of subcortical heterotopia associated with EML1 mutations remain unknown. Using a forebrain-specific mouse model and mutant human cells, this work innovatively demonstrates that by restoring microtubule function, abnormal progenitor distribution and heterotopic volume are significantly reduced.

Garde et al. comprehensively reveal how feedback regulates the heat shock response (HSR), a universally conserved gene expression program enabling cellular adaptation to stress. The HSR consists of a core feedback loop governing the expression of the chaperone Hsp70 reinforced by a stress-dependent auxiliary feedback loop controlling Hsp70 subcellular localization.

Du et al. identify Sec23IP as an adaptor that recruits VPS13B to ER exit site–Golgi interfaces, and the interaction is required for the formation of tubular ERGIC and efficient ER export of procollagen. These findings reveal a role of VPS13B–Sec23IP interaction in Cohen syndrome pathogenesis.

Axonal regeneration is an energy-demanding process. Masin et al. show that in Pten and Socs3 co-deleted retinal ganglion cells, axonal regrowth requires and is fueled by a local axonal upregulation of glycolysis. Its targeting could provide new therapeutic avenues to induce axonal regrowth.

Novel in vitro assays reveal that perilipins, abundant lipid droplet proteins, differ in their sensitivity to phospholipid density of the lipid droplet monolayer, explaining how proteins distinguish between different lipid droplet populations. The work demonstrates that perilipin 3 and 4 can replace the phospholipid monolayer.

This study unveils migratory autolysosome disposal, a response to lysosomal damage where cells expel LAMP1-LC3 positive structures via autolysosome exocytosis, requiring autophagy machinery, SNARE proteins, and cell migration. This novel mechanism highlights the intricate relationship between cell migration, organelle quality control, and extracellular vesicle release.

Silverman et al. leveraged advanced light and electron microscopy to perform quantitative morphometry of the intestinal tuft cell cytoskeleton. Three-dimensional reconstructions of segmented image data reveal a co-aligned actin–microtubule superstructure that may play a fundamental role in tuft cell function.

de Leeuw, Budhathoki, and colleagues examine the mechanical limitations that nuclear volumes impose on epithelial remodeling in Drosophila. They identify two primary mechanisms—nuclear dispersion and nuclear deformation—that permit the resolution of internuclear tensions. Failures in both pathways lead to epithelial extrusion.

In this study, West et al. define roles for Cldn7 during breast cancer invasion and metastasis. They show that Cldn7 restricts aggressive breast cancer cell behaviors by suppressing proinvasive gene expression programs, such as induction of smooth muscle actin–related genes.

Ugur et al. characterize the bridge-like lipid transfer protein VPS13B and report its localization between Golgi cisternae and its impact on Golgi complex reformation after its BFA-induced dispersion. They also provide evidence for its functional partnership with FAM177A1, a newly identified Golgi complex protein.