On the cover
A dorsal view of a Drosophila pupa expressing a GFP fusion protein in its peripheral nervous system shows both the eyes and the sensory bristles that dot the head, thorax, and abdomen of the fly. Upadhyay et al. reveal how a protein called Sanpodo regulates bristle development by activating Notch signaling in some precursor cells while suppressing it in others.
Image © 2013 Upadhyay et al.
See page 439.
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Cells with reduced origin firing have an increased rate of replication fork progression, whereas fork progression is slowed in cells with excess origins.
The loss of the spindle checkpoint protein Bub3 is sufficient to induce aneuploidy and drive tumorigenesis when apoptosis is compromised.
DNA synthesis by Pol η promotes fragile site stability by preventing under-replicated DNA in mitosis
Pol η–dependent DNA synthesis at stalled replication forks during S phase suppresses chronic fragile site instability by preventing checkpoint-blind under-replicated DNA in mitosis.
Heterochromatin protein 1 promotes self-renewal and triggers regenerative proliferation in adult stem cells
The planarian chromatin regulator HP1, at least in part acting through increased expression of Mcm5, inhibits differentiation of adult stem cells and triggers their proliferation in response to injury.
IFN-γ induces the interaction of HDAC1 and p53, leading to p53 deacetylation, which facilitates autophagy via Bmf suppression.
Sanpodo controls sensory organ precursor fate by directing Notch trafficking and binding γ-secretase
In sensory organ precursor cells, Sanpodo can enhance or suppress Notch signaling by promoting interaction with Presenilin or driving receptor internalization, respectively.
Release of cellular tension signals self-restorative ventral lamellipodia to heal barrier micro-wounds
Endothelial and epithelial barrier disruptions are detected via local decrease in cellular tension, which are coupled to reactive oxygen species–dependent self-restorative actin remodeling dynamics.
Metalloproteinase-mediated cleavage of EphA2 induces breast tumor cells to shift from collective invasion to single-cell invasion.