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Wound made to a GFP-actin-expressing Drosophila melanogaster embryo, showing an actin cable running around the wound periphery and filopodia extending from the wound-edge cells.
After exocytosis, synaptic vesicles are reformed by slow clathrin-mediated endocytosis. However, evidence also supports the existence of faster retreival mechanisms in neurons, including 'kiss-and-run', where vesicles fuse only partially with the presynaptic membrane before being retrieved. New insights in synaptic vesicle dynamics have been obtained from vesicle imaging and from studies with mutant animals. Recently, measurements of capacitance changes induced by the fusion of single synaptic vesicles in synapses corroborate the hypothesis that kiss-and-run operates in neurons. Here, we review the evidence supporting fast vesicle retrieval and evaluate its role in neurotransmitter release.
The organization of signalling complexes represents the coalescence of cell biology and signal transduction. Recent work on Dishevelled (Dvl), a multifunctional component of the Wnt–Frizzled (Fz) signalling pathway, ascribes vesicle- and actin-binding properties to a single domain within the protein. This could represent a critical point for divergence of the Wnt signalling pathway.
The combined use of laser ablation and live imaging in Drosophila melanogaster embryos provides new ways to visualize the dynamics of wound healing. Analysis of lesions made in living embryos mutant for small GTPases reveal distinct and unexpected roles for actin cables and protrusions in wound repair. Hole closure is definitely more complex than simply pulling a string.
Neuregulin (NRG) is a crucial regulator of oligodendrocyte development, strongly promoting both the proliferation of oligodendrocyte precursor cells and the survival and maturation of oligodendrocytes. How can the same growth factor mediate such different effects? New work in this issue of Nature Cell Biology implicates an integrin-mediated switch in signalling that results in the loss of the proliferative response and the enhancement of survival and maturation.
The Chk2 checkpoint kinase is implicated in radiation-induced apoptosis. New findings suggest that radiation induces dissociation of Chk2 from the promyelocytic leukemia gene product (PML). Thus, PML nuclear bodies may function as regulated storage depots, releasing specific proteins in response to specific types of cellular stress.