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Autophagy is a cellular degradation and recycling process with complex roles in health and disease and emerging relevance to translational research. In this issue, we launch a Series of commissioned articles that will discuss recent advances and outstanding questions driving this rapidly expanding and diverse field.
Inflammation and reactive oxygen species (ROS) production after central nervous system injury are thought to enhance tissue damage and hamper neuronal regeneration. Evidence now suggests that NADPH2 oxidase delivery from macrophages to injured neurons through extracellular vesicles, promotes ROS signalling and axon recovery.
Cytoplasmic flows are essential for various cellular processes. However, tools to manipulate these flows within cells are still lacking. Now research shows that an optical tool allows for control of cytoplasmic flows and can be used as a subcellular rheometer.
Exosomes are heterogeneous, nanoscale vesicles that mediate cellular communication. A study now leverages a size separation strategy to identify sub-classes of nanoparticles, revealing a subtype without an encapsulating membrane and variation in vesicle cargo, suggesting that size is not the only driver of heterogeneity.
N6-methyladenosine (m6A) mRNA modification influences mRNA fate by stimulating recruitment of m6A reader proteins. A previously unappreciated class of m6A reader proteins is now shown to use a common RNA-binding domain and flanking regions to selectively bind m6A-containing mRNAs, increasing their translation and stability.
In this Review Article, Klionsky and co-authors discuss selective autophagy pathways that degrade unwanted cytosolic components and organelles, and how these pathways require ligand receptors and scaffold proteins for cargo specificity.
Autophagy and cancer: In this Review, Galluzzi and colleagues discuss the cellular and molecular mechanisms whereby autophagy functions in multiple aspects of malignant disease, including cancer initiation, progression and responses to therapy.
van Haren et al. develop a tool to rapidly dissociate proteins from the growing end of microtubules through photo-induced disassembly of end-binding protein 1 (EB1), and find that this reduces microtubule growth and alters cell migration.
Using nanopillars with increased spatial resolution, Shiu et al. identify high perinuclear forces that originate from contractile apical actin filaments that span across the nucleus and are dependent on lamin A and the LINC complex.
Hawk et al. show that RIPK1 activation during extracellular matrix detachment induces mitophagy through mitochondrial phosphatase PGAM5 to increase reactive oxygen species and non-apoptotic cell death, and that antagonizing RIPK1/PGAM5 enhances tumour formation.
Zajac et al. show that in colorectal cancer, decreased TGF-β signalling promotes apical actomyosin contractility and collective apical budding of invading tumour spheres with inverted polarity that drive metastatic spread.
Hervera et al. show that extracellular vesicles containing NOX2 complexes are released from macrophages and incorporated into injured axons, leading to axonal regeneration through PI3K–p-Akt signalling.
Lyden and colleagues use asymmetric flow field-flow fractionation to classify nanoparticles derived from cell lines and human samples, including previously uncharacterized large, Exo-L and small, Exo-S, exosome subsets.
Mittasch et al. show that controlling cytoplasmic flow via focused-light-induced cytoplasmic streaming (FLUCS), a non-invasive technique, can be used to invert asymmetric cell division in Caenorhabditis elegans zygotes.
Ahier et al. describe a method to isolate intact mitochondria from specific cells in Caenorhabditis elegans and show that the germline is more prone to propagating deleterious mitochondrial genomes than somatic lineages.