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    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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ISSN 0021-9525
EISSN 1540-8140
In this Issue

In This Issue

In Focus

Study shows that lamellipodia allow cells to move in a specific direction.

People & Ideas

Ohsumi's work continues to provide much of the foundation for our current understanding of autophagy.


The cell biology of disease


SUMOylation of the ubiquitin ligase HERC2 promotes efficient chromatin licensing in the vicinity of 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.

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.

Munc13-4 is a Ca2+-dependent membrane- and SNARE-binding protein that promotes membrane fusion.

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.

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