Issues

Antagonism between RhoA and Rac1 pathways creates cell heterogeneity that aids epidermal morphogenesis.

Dekker investigates the three-dimensional organization of the genome.

Beirowski et al. discuss a new study that reports that PLP-deficient myelin fails to provide metabolic support to axons, leading to degeneration.

Farhan discusses Scharaw et al.’s study about how the COPII machinery is used to replenish EGFR at the cell surface.

Sun, Guo, and Fässler review the function and regulation of integrin-mediated mechanotransduction and discuss how its dysregulation impacts cancer progession.

Basal bodies (BBs) organize and anchor motile cilia. This study uncovers components that asymmetrically localize to the rotationally symmetric BBs, where they fortify specific BB domains. Asymmetrically localized BB components are necessary to resist asymmetric ciliary forces.

Stereocilia of the inner ear’s sensory hair cells are filled with a paracrystalline array of parallel actin filaments. Krey et al. show that the actin cross-linker plastin-1 is needed for random liquid packing of actin filaments and final stereocilia diameter.

Antagonism between the GTPases Rac1 and RhoA controls different morphogenetic processes during embryonic development. Martin et al. use quantitative imaging analyses to demonstrate that cell-autonomous antagonism between the RhoA- and Rac1-like pathways defines cell-to-cell heterogeneity during epidermal morphogenesis in Caenorhabditis elegans.

Rab GTPases control vesicle formation and transport, but which proteins are important for their regulation is incompletely understood. Thomas and Fromme provide definitive evidence that TRAPPII is a GEF for the yeast Rab11 homologues Ypt31/32 and implicate the GTPase Arf1 in TRAPPII recruitment, suggesting that a bidirectional cross talk mechanism drives vesicle biogenesis.

Joshi et al. show that Pex30p and Pex31p contain reticulon-like ER tubulating domains. Like reticulons, they localize to the edges of ER sheets and tubules but are only present in subdomains. These subdomains are devoid of reticulons and are the sites of pre-peroxisome vesicle biogenesis.

The authors show that central nervous system myelin lacking proteolipid protein (PLP) induces mitochondrial dysfunction, including altered motility, degeneration, and ectopic smooth endoplasmic reticulum interactions, leading to axonal structural defects and degeneration. Mutated PLP occurs in hereditary spastic paraplegia, and these cellular effects provide potential insight into the pathology of the disease.

Maintenance of EGFR plasma membrane levels is critical for cell functioning. Scharaw et al. demonstrate that endosomal RNF11 is required for transcriptional up-regulation of COPII components, specifically facilitating EGFR transport in response to its lysosomal degradation after EGF stimulation.

Nishimura et al. show that DAAM1, a formin family actin polymerization regulator, stabilizes epithelial cell junctions by counteracting the WAVE complex, another actin regulator. Loss of DAAM1 promotes the motility of junctional membranes and thereby enhances their invasion of neighboring environments.

Few tools exist to examine the inner nuclear membrane (INM) in living cells, and the INM-specific proteome is poorly characterized. Smoyer et al. combine a split-GFP screen and fluorescence correlation spectroscopy analysis to identify membrane proteins that access the INM and study INM-specific interactions.