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    Temporal changes in the levels of an inhibitor called DIAP1 allow caspases to promote the elongation of sensory organ shaft cells without inducing their death. Inappropriate degradation of DIAP1 causes cell death and a loss of sensory bristles.
    See page 219.

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ISSN 0021-9525
EISSN 1540-8140
In this Issue

In This Issue

In Focus

Two homologues of the cohesin protein Scc3 have specialized roles in chromatid cohesion.

People & Ideas

Senthil Muthuswamy uses 3D cell culture to explore the influence of cell polarity on oncogenic transformation.




In vertebrates, two Scc3 homologues control sister chromatid cohesion of distinct chromosomal regions.

Removal of the entire keratin family of intermediate filament proteins from embryonic epithelia has surprising implications for mTOR signaling.


Telomeres fail to attach to the nuclear envelope and lose structural integrity in cells lacking SMC1β.

Loss of ubiquilin or erasin activates ER stress, increases accumulation of polyubiquitinated proteins, and shortens lifespan in worms.

Caspase activation is regulated by the turnover of E3 ubiquitin ligase, DIAP1, and depends on cell type and maturity.

Pex3 links peroxisome formation and inheritance. By binding to class V myosin, biogenesis protein Pex3 also directs the organelles into daughter cells.

The clathrin adaptor protein AP-1 and the motor KIF13A work together to deliver cargo into maturing melanosomes.

Neighbor of BRCA1 (NBR1) suppresses growth factor responses by redirecting activated receptors to lysosomes for degradation.

Neuronal Ca levels are regulated by glutamate receptor activation, which recruits PIKfyve to voltage-gated Ca channels, prompting their degradation.

Analogous to synaptotagmin 1, a calcium-sensitive regulator of presynaptic vesicle fusion, synaptotagmin 4 needs both of its calcium-binding sites to regulate synaptic plasticity via postsynaptic retrograde signaling.

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