On the cover
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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The actin-binding protein ADD1 associates with mitotic spindles through Myo10 and is crucial for proper spindle assembly and mitotic progression.
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.
Dbl3 drives Cdc42 signaling at the apical margin to regulate junction position and apical differentiation
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.