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    β-Galactosidase activity (blue) indicates senescent cells in the liver of hyperthyroid mice. Zambrano et al. describe how thyroid hormone and its receptor cause increased mitochondrial respiration and reactive oxygen species production, leading to DNA damage and premature cell senescence.
    Image © 2014 Zambrano et al.
    See page 129.

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ISSN 0021-9525
EISSN 1540-8140
In this Issue

In This Issue

In Focus

Repair protein helps resolve entanglements between sister chromatids.

People & Ideas

Kozlov studies the biophysics of membrane shape and behavior.

Review

Report

The actin-binding protein ADD1 associates with mitotic spindles through Myo10 and is crucial for proper spindle assembly and mitotic progression.

Article

Coupling of replication fork speed and PCNA unloading to nucleosome assembly may maintain chromatin integrity during transient histone shortage.

TopBP1/Dpb11 prevents accumulation of anaphase chromatin bridges by stimulating the Mec1/ATR kinase and suppressing homologous recombination.

A long noncoding RNA directly builds an intrachromosomal interaction complex to establish allele-specific transcriptional gene silencing over a large chromosomal domain.

Phosphorylation of synaptic cytoskeletal components by casein kinase 2 promotes the development and maintenance of synaptic connections.

Post-translational methylation of the non-histone, actin-binding protein EF1α1 is essential for neural crest migration.

The guanine nucleotide exchange factor Dbl3 promotes spatially restricted Cdc42 activation in the apical zone, regulating apical morphogenesis and tight junction positioning.

Thyroid hormone and its receptor act in concert with NRF1 to increase cellular respiration and reactive oxygen species production, leading to DNA damage and premature senescence in susceptible cells.

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