People & Ideas
Lipotoxicity is frequently associated with alkalinization of lysosomes and impaired autophagic flux but the relationship between the two is unclear. Trudeau et al. show that autophagic flux can be restored in β islet cells chronically exposed to fatty acids by re-acidification of lysosomes with photoactivatable nanoparticles.
Ephs interact with ESCRT complex components and are released via extracellular vesicles or exosomes. EphB2 released via exosomes mediates a novel cell contact–independent mode of ephrin-Eph signaling that contributes to axon guidance in cell–cell repulsion processes.
The Sam68 nuclear body is composed of two RNase-sensitive substructures joined by the adaptor HNRNPL
Some nuclear bodies are formed with an architectural RNA (arcRNA) as the structural core. Here, Mannen et al. screened for new nuclear bodies built on unidentified arcRNAs and found that the Sam68 nuclear body (SNB) is composed of two distinct RNase-sensitive substructures. HNRNPL acts as the adaptor to combine the two substructures, thus forming the full SNB.
Sec16A is known to be required for COPII vesicle formation from the ER. Here, Bruno et al. show that, independent of its role at the ER, Sec16A is a RAB10 effector involved in the insulin-stimulated formation of specialized transport vesicles that ferry the GLUT4 glucose transporter to the plasma membrane of adipocytes.
Phosphatidylethanolamine, an essential phospholipid for mitochondrial functions, is synthesized at the mitochondrial inner membrane. Miyata et al. demonstrate that Ups2–Mdm35, a protein complex in the mitochondrial intermembrane space, mediates phosphatidylserine transport for phosphatidylethanolamine synthesis in respiration-active mitochondria of Saccharomyces cerevisiae.
Ciliogenesis in differentiating epidermal cells correlates with activation of Notch signaling, which requires Presenilin-2 targeting to basal bodies/cilia. Ezratty et al. show that the GTPase ARF4 regulates Presenilin-2 localization and subsequent Notch-dependent differentiation, suggesting that polarized exocytosis to basal bodies spatially regulates Notch signaling during skin development.
Zhou et al. show that reduced mitochondrial motility and energy deficits in injured axons are intrinsic mechanisms contributing to regeneration failure in mature neurons.