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Lo et al. show that Cavin4 plays a role in skeletal muscle T-tubule formation and maturation. Without Cavin4, Cav3 and caveolae accumulate in the T-tubules, which then fragment. Cavin4 is recruited by Bin1 to developing T-tubules and is required for the recycling of Cav3/caveolae back to the sarcolemma as muscle matures.

G protein–coupled receptors (GPCRs), upon serine–threonine phosphorylation, undergo recycling or degradation. Anwar et al. demonstrate a new fate of GPCRs, exemplified by tyrosine phosphorylated sphingosine-1-phosphate receptor 1 (Y143S1PR1), which through its interaction with BiP, is routed to the endoplasmic reticulum where it dysregulates S1P-induced Ca2+ signaling and barrier function.

Rabas et al. describe a novel means of intercellular communication in which processes evoked to mitigate cytotoxicity in metabolically stressed cells can promote PINK1-dependent packaging of mitochondrial DNA into exosomes to evoke invasive behavior in other cells.

Hu et al. demonstrate that transgenic expression of Glypican 4 (Gpc4) in the endoderm rescues convergence and extension (C&E) defects in all germ layers in gpc4−/− embryos. The rescue of mesoderm is mediated by Wnt5b and Wnt11f2 and depends on signaling filopodia.

Neurons use different modes of endocytosis at synapses to maintain reliable communication across varying neural activities. This study shows that the Minibrain kinase and calcineurin switch the predominant mode of endocytosis during moderate and intense stimuli by regulating the phosphoinositol phosphatase activity of synaptojanin.

Sengupta et al. report the high-resolution cryo-EM structure of oligomeric VCC in a near-physiological lipid bilayer environment. Three distinct structural states indicate the conformational flexibility of the β-PFT in membranes, which may potentially guide the pore formation mechanism.

Herbst et al. use a novel approach for identifying activity-dependent changes in the nuclear proteome of neurons and provide evidence that regulated degradation of the tumor suppressor protein PDCD4 is required for normal activity-dependent transcription in neurons.

Clay et al. show that cells with DNA breaks that persist into mitosis activate sustained DNA damage signaling, regulated by Fanconi anemia proteins and the alternative end-joining repair protein DNA polymerase θ. This signaling enables broken chromosome segregation and prevents micronuclei.

Sarangapani, Koch, Nelson et al. show that phosphorylation by the conserved Mps1 kinase reduces kinetochore–microtubule attachment strength using a reconstitution system. Mps1 phosphorylates Ndc80, a microtubule-binding protein in the kinetochore, to aid mitotic error correction in cells and ensure accurate chromosome segregation.

Otto et al. show that the cortical ER undergoes programmed collapse from the plasma membrane during meiosis. Collapse separates the ER into distinct populations and determines which regions are eligible for inheritance by gametes and which are degraded by mechanisms including Atg40-mediated autophagy.

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