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    Cover Image

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    On the cover
    Cane et al. reveal that overexpression of the chromokinesin motor NOD (red) stabilizes aberrant interactions between kinetochores and spindle microtubules (green), resulting in the incorrect attachment of sister chromatids to microtubules emanating from the same spindle pole.
    Image courtesy of Tom Maresca.
    See page 203.

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ISSN 0021-9525
EISSN 1540-8140
In this Issue

In This Issue

In Focus

Enzyme helps cancer cells reactivate repair mechanism and overcome loss of tumor suppressor.

People & Ideas

Reck-Peterson studies the mechanism and regulation of dynein’s motor activity.



Enzymatic activity of the UvrD DNA helicase FBH1 is required for the efficient induction of DSBs and apoptosis specifically in response to DNA replication stress.

The chromosome-centered RanGTP gradient, which is strongly reduced in slow-growing normal cells, is amplified by chromosomal gain and is required for mitosis in rapidly growing aneuploid cells.

PINK1 activates the HECT-like E3 ubiquitin ligase activity and self-association of Parkin upstream of its translocation to mitochondria and induction of mitophagy.


Ligase IV, but not its catalytic function, is required for DNA-PK–dependent end synapsis during nonhomologous end joining.

Cathepsin L degrades 53BP1 to overcome genomic instability and growth arrest in BRCA1-deficient and triple-negative breast cancers.

Polar ejection forces, which push chromosomes away from spindle poles, modulate kinetochore–microtubule attachment stability.

Perlecan/Trol at the neuromuscular junction suppresses presynaptic canonical Wg signaling but enhances the postsynaptic Frizzled nuclear import pathway.

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