On the cover
Suraneni et al. reveal that fibroblasts require the Arp2/3 complex to form lamellipodia and undergo sustained directional migration. A wild-type cell (top right) spreads onto a surface by extending broad, ruffle-like lamellipodia rich in F-actin (red), whereas a cell lacking the Arp2/3 subunit ARPC3 (bottom left) forms thin, filopodia-like protrusions containing actin bundles.
Image courtesy of Parveen Suraneni.
See page 239.
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People & Ideas
The cell biology of disease
DNA damage–inducible SUMOylation of HERC2 promotes RNF8 binding via a novel SUMO-binding Zinc finger
SUMOylation of the ubiquitin ligase HERC2 promotes efficient chromatin licensing in the vicinity of DNA double-strand breaks.
Human RNF169 is a negative regulator of the ubiquitin-dependent response to DNA double-strand breaks
RNF169 competes with repair factors to bind to ubiquitylated chromatin at sites of DNA damage, influencing repair pathway utilization.
The BRCA1 tumor suppressor associates with both the DROSHA microRNA maturation complex and primary miRNA transcripts, and promotes transcript processing.
Budding yeast Sey1p functions analogously to mammalian atlastins in mediating ER fusion through a mechanism that is redundant with a second, ER SNARE-mediated fusion mechanism.
Retrieval of β integrins from the lysosomal degradation pathway mediated by sorting nexin-17 is important for integrin recycling and regulation of cell migration.
MCAK activity at microtubule tips regulates spindle microtubule length to promote robust kinetochore attachment
The kinesin MCAK binds to end-binding proteins and antagonizes centrosome separation and promotes robust kinetochore attachments to spindle microtubules.
Embryonic stem cell–derived fibroblasts with genetic disruption of the Arp2/3 complex are unable to form lamellipodia or undergo sustained directional migration.
Human telomere replication initiates either from within telomere repeats or from within the subtelomere using a chromosome-specific replication program that appears conserved between different cell types.
In addition to its role in DNA lesion recognition, the damaged DNA-binding protein DDB2 elicits unfolding of large-scale chromatin structure independently of the CRL4 ubiquitin ligase complex.
Loss of the telomere component TRF1 and the DNA repair mediator 53BP1 enhances the ATR-mediated DNA damage response, promotes the homology-directed repair of dysfunctional telomeres, and exacerbates DNA damage.
In contrast to vertebrate CBY, which functions in WNT signaling, Drosophila CBY is essential for normal basal body structure and function but dispensable for Wg signaling.
Positional information, independent of neuronal activity, regulates presynaptic strength, with the strongest presynaptic terminals closest to the soma.