On the cover
Lewellyn et al. describe how the protein kinase Misshapen decreases integrin levels to promote the migration of follicle cells during Drosophila egg chamber morphogenesis. In an egg chamber stained for cortical actin (red), wild-type follicle cells (marked with GFP, green) break away from a group of immotile, Misshapen-null cells and bisect the oocyte by invading the inner germ cell cluster.
Image © 2013 Lewellyn et al.
See page 721.
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Processing of unusual replication intermediates such as reversed forks by MUS81 contributes to oncogene-induced double-strand breaks and depends on mitotic entry.
Rer1p is an ER/cis-Golgi membrane protein that maintains ciliary length and function by reducing γ-secretase complex assembly and activity (thereby balancing Notch signaling) and increasing Foxj1a expression.
Misshapen decreases integrin levels to promote epithelial motility and planar polarity in Drosophila
Misshapen promotes individual cell motility in the Drosophila follicular epithelium through a mechanism that appears to reduce integrin levels at each cell’s trailing edge.
Cortical layer 5 pyramidal neurons and spinal cord motor neurons are selectively vulnerable to degeneration after loss of the autophagy gene Epg5.
CUL4B up-regulates CDK2 by repressing miR-372 and miR-373, leading to increased phosphorylation and stabilization of CDC6, thus promoting replication licensing.
During mitosis, cohesin- and condensin-based pericentric chromatin loops function as a spring network to balance spindle microtubule force.
MISP is a substrate of Plk1 and important for the stabilization of cortical and astral microtubule attachments to regulate mitotic spindle positioning.
After acidic organelles induce signaling to activate ER calcium ion release, local microdomains of high calcium at ER–acidic organelle junctions feed back to activate further acidic organelle calcium release.
Sicily, which was identified in a screen for proteins involved in neurodegeneration, interacts with cytosolic Hsp90 to chaperone the complex I subunit ND42, before its mitochondrial import.
Vps35 loss promotes hyperresorptive osteoclastogenesis and osteoporosis via sustained RANKL signaling
Vps35 deficiency leads to impaired RANK trafficking, enhanced RANKL signaling, increased osteoclastogenesis and function, and osteoporotic deficits.
Unprecedented proteome plasticity in response to stress in yeast is revealed using a novel screening platform that allows tracking of protein localization and abundance at single-cell resolution.